History and examination

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4 History and examination

image Clinical cases for thought

Case 4.1

A 54-year-old woman presents to your office via referral from her cardiologist. She has a spectrum of complaints including irregular heart beat, dizziness on standing, feelings of hot and cold in her arms and feet, and stomach upset including irregular bowel movements through the day. She has had a complete cardiac work-up done by her cardiologist in which all findings were normal. The cardiologist feels that this patient may be suffering from a form of dysautonomia.

Questions

• 4.1.1 Which cranial nerves can you examine that will give you information about the level of function of her parasympathetic nervous system? Which tests would you perform?

• 4.1.2 What examinations would you perform to evaluate the level of function of her sympathetic nervous system?

• 4.1.3 What is dermatographia and in what situations would you expect to find it?

Case 4.2

A 23-year-old male presents to your office with double vision and headaches. On examination you discover that he has an exophoria of the right pupil.

Questions

• 4.2.1 What are the causes of exophoria? What is exotropia?

• 4.2.2 How would you differentiate between a weak medial rectus muscle and an overactive lateral rectus muscle?

Introduction

The neurological examination is traditionally taught using a disease or ablative lesion-orientated model. While this approach may help to detect the presence of both serious and benign disorders, it is less helpful for the practitioner who wishes to investigate and estimate the physiological functional integrity of the nervous system. A more functional approach to the neurological examination heightens the examiner’s sensitivity to physiological aberrations responsible for the vast majority of neurological symptoms. At the same time, a practitioner using this approach is more likely to detect subtle signs of pathology.

The practitioner who intends to utilise the functional approach of examination must be concerned with the identification of ablative lesions and the presence of disease processes, but must also attempt to identify any physiological lesions manifesting themselves as subclinical physical symptoms.

For example, if a patient presents with a recent history of an inner ear infection complicated by hearing loss and balance disturbances, one might assume the possibility of potential damage to the vestibular and/or cochlear hair cells, which are the receptors responsible for balance and hearing. At follow-up after a course of antibiotics, a commonly occurring scenario is that the patient states that their hearing has returned and their balance is no longer a concern to them but they are starting to experience migraines, which they had not experienced before. The vestibular system can have a profound influence on peripheral resistance due to disynaptic or polysynaptic connections between vestibular neurons and the tonic vasomotor neurons of the rostral ventrolateral medulla. The purpose of these connections is for protection against orthostatic stress. Should a comprehensive examination focused on the functional state of the vestibular-cerebellar and medullary areas show dysfunction or asymmetry of function in this patient, it would be of great value to the patient for you to address the central consequences of the inner ear infection and attempt to reduce the vasomotor dysregulation that has no doubt developed during the course of their illness. Treatment, involving appropriate afferent stimulation and exercises aimed at restoring symmetry and integrity to the vestibular system and associated brainstem nuclei, should be a primary consideration in this patient’s management, in addition to any pharmaceutical approach also applied.

In learning the traditional approach to the neurological examination a student or inexperienced practitioner may be less interested in minor asymmetries of cranial nerve function or motor and sensory signs, especially when the history does not alert to serious pathology. This is not the case in the functional examination where minor asymmetries or altered functional output are of great significance in the analysis of the physiological lesion. Each test must be performed with alert observational skills and meticulous care, comparing the results bilaterally when possible.

The functional neurological examination aims to elicit information about mental, sensory, and motor functions. Sensory functions are analysed by observing the patient’s mental or motor response to stimulation of the various sensory receptors in the head and body. Motor functions are analysed by observing the patient’s requested or spontaneous volitional actions. Sensory and motor functions can also be analysed by observing both muscle and glandular responses to sensory stimulation. The muscles and glands are the final common effector systems of the body. Their responses are normally dependent on the output from complex neuronal integration and, as such, can be utilised in assessment of the functional state of the neuron pools that control their output. Reflexogenic systems, such as opticokinetic stimulation and vestibulo-occular stimulation can also be utilised in gaining an understanding of the patient’s functional state.

The five parameters of effector response are important clues in gauging the cis of upstream neuron systems

image Quick facts 4.1

Central integrative state (cis) is dependent on the following

1. Fuel delivery

2. FOF of presynaptic pools

image Quick facts 4.2

Energy production in the cell

1. Glycolysis

2. Citric acid cycle

3. Electron transport chain

The response of an effector (e.g. muscle) to a stimulus or command is largely dependent on the central integrative state (CIS) of the presynaptic neuronal pool projecting to the motor neuron of the effector. Therefore, the CIS of a neuronal pool can be predicted or estimated by observing the characteristics of the motor response of the downstream motor neuron to a unit stimulus. The parameters of the effector response observed can be summarised under the following observational findings:

1. Latency and velocity of the response

2. Amplitude of the response

3. Smoothness of movement of the response

4. Fatigability of the response and

5. Direction of the response.

All of the responses observed during the functional examinations performed on a patient, should be evaluated with the above parameters in mind. It is also important to visualise the pathways actively involved in producing the actions that one is examining. This allows the practitioner the advantage of performing additional or more detailed tests directed at the same pathways throughout the examination should disparities in the patient’s responses become apparent.

Latency and velocity of a response

The latency refers to the time between the presentation of a stimulus and the motor, sensory, autonomic, or behavioural response of the patient. This provides information concerning conduction time along nerve axons and spatial and temporal summation occurring in the neurons involved in the functional action chain of the response. The velocity of the response is another window of spatial and temporal summation and conduction time.

image Quick facts 4.3

Diagnostic approach

1. Serious disorders

2. Common disorders

3. Underlying issues

4. Masquerades

5. Level of the lesion

6. Frequency of firing (FOF)

7. Fuel delivery

The time to summation (TTS) and time to peak summation (TTSp) are terms that describe, respectively, the latency and average velocity of effector responses. The pupillary action observed in response to a light stimulus offers a good illustration of these concepts. Under normal conditions, the pupils will respond with a relatively equal TTS and TTSp in both eyes when stimulated with an equal light stimulus. However, in the situation where the central integrative state of the neurons in the right Edinger–Westphal nucleus or mesencephalic reticular formation is further away from threshold, the TTS of the right eye would be expected to be increased from that of the left. The same result may be expected when measuring the velocity of the response, or an increased time to maximal pupil constriction (increased TTSp). The same result, that is increased TTS and TTSp in the right eye, may be found with an afferent pupil defect such as would occur if the right eye end organ was impeded by a photoreceptor or axonal conduction deficit such as in retinal or optic nerve dysfunction. Thus there is the need for a complete fundoscopic and visual acuity examination when unequal pupil responses are present.

Amplitude of a response

The amplitude of the response refers to the maximum change in the parameters being assessed. This can be a useful indicator of the relative frequency of firing in a neuronal pool: for example, the degree of excursion of the eye during the smooth phase of pursuit movement during optokinetic testing of eye movements; or, in keeping with our first example, the maximum change in pupil size when testing the pupil light reflex.

Smoothness of a response

Smoothness of any movement is dependent on complex interactions between multiple neuronal pools. An example is the smoothness of visual tracking in the horizontal plane. This requires complex interactions between the cerebellum, vestibular system, neural integrator, and occipital, parietal, and frontal lobes. A poor central integrative state in any of these areas may affect the quality of visual tracking in one or more directions. Specific features of the visual tracking deficit may alert to greater involvement of one area over another. Uncoordinated or jerky movements are referred to as dysmetric.

Fatigability of a response

This refers to the ability to maintain a response during continued or repeated presentation of a stimulus. A progressive reduction in ocular roll and skew deviation between successive head tilts is an example of increasing fatigue of the ocular tilt reaction (OTR). Poor maintenance of a response reflects increased fatigability. The fatigability coefficient is an arbitrary descriptor of the fatigability of a neuronal pool.

Direction of a response

image Quick facts 4.4

Five components of effector response

1. Latency and velocity

2. Amplitude

3. Smoothness

4. Fatigability

5. Direction

The direction of response elicited is compared to the expected normal response to provide further information about the integrity of a neuronal pool. For example, the direction of change of pupil size when shining a light in the eye, the direction of nystagmus during caloric irrigation of the ear, and the direction of change of skin temperature in response to a cognitive task or vestibular stimulation all have an expected normal response direction. If the direction of response is different from the expected outcome, this may indicate the presence of pathology, fatigue, or plastic alterations in neural circuitry.

The longitudinal level of the lesion

When examining a patient, the practitioner needs to consider that dysfunction at any level of the pathway, from the sensory receptor to the effector, may result in aberrant findings during an examination of body function. The usually considered longitudinal levels that may be involved in a dysfunctional output response include the following: the receptor or effector, the afferent or efferent pathways of the peripheral nerve, the spinal cord, the brainstem or cerebellum, the thalamus or basal ganglia, the cortex. It is important to remember that a dysfunction at one longitudinal level of the neuraxis may result in dysfunction at other levels also.

The following example illustrates the concept. A patient presents with unilateral ptosis. The cause of the ptosis might be occurring at the effector level involving the ACh receptors of the orbicularis oculi muscle as in myasthenia gravis. The cause of the ptosis might be occurring at the peripheral nerve level as could occur in a partial third nerve compression palsy. The cause of the ptosis may involve disruption of the sympathetic fibres to the levator palpebrae superiorus muscle at any point along the sympathetic projections from the hypothalamus, through the spinal cord, the superior cervical ganglia, and postsynaptic projections that follow the oculomotor nerve to the muscle as in Horner’s syndrome. Alternatively, it may be caused by asymmetric cortical output resulting in overstimulation of the pontomedullary reticular formation (PMRF), which has inhibited sympathetic output to the eyelid.

A complete history and examination of the patient would enable the correct diagnosis without too much difficulty in this case.

Approaches to developing a differential diagnosis

image Quick facts 4.5

The basic functional neurological examination

• Blind spots and visual fields

• Pupil size and PLRs (pupil light reflexes)

• Motor and sensory examination of the head

• Motor and sensory examination of the trunk and limbs

• Skin and tympanic temperature patterns

• Ophthalmoscopic/otoscopic examination

• Vestibular, cerebellar, and spatial awareness tests and

• Specific cortical tests.

Before discussing the history and physical examination procedures in general, it is necessary to give some thought to the reason for performing these activities in the first place. The history and physical examination are procedures that allow the practitioner to develop a clinical impression of the state of health or disease of the patient. Based on the clinical impression, the practitioner then arrives at a working diagnosis of the patient’s condition and develops the most appropriate approach to treatment of the patient.

The process of arriving at a diagnosis usually first involves the development of a differential diagnosis, which is the consideration of a number of alternative diagnostic possibilities in light of the history. The list of differential diagnoses is then systematically reduced by the results obtained from further tests performed on the patient. The most common tests utilised clinically include the examination procedures that compose the physical examination, laboratory blood or body fluid analysis, diagnostic imaging such as plain film X-rays, MRI, fMRI, or PET scans, and electrophysiological evaluations such as qEEG, EEG, and EMG.

Space limitations only allow for a brief overview and suggested approach to differential diagnosis at this time, but several excellent texts on the subject can be found in the additional reading section at the end of the chapter.

One approach to developing a differential diagnosis is to consider the possible causes of the patient’s presenting symptom picture with respect to a list of major classifications of pathological processes. The major classifications include vascular disorders, infectious conditions, neoplastic disorders, neurological disorders, degenerative disorders, inflammatory disorders, congenital disorders, connective tissue disorders, autoimmune disorders, trauma, endocrine disorders, and soft tissue disorders. The pneumonic VINDICATES can be used to remember the major classifications for this approach.

Once a clear history has been taken from the patient, possibilities from each category can be considered and analysed in light of the symptom picture that the patient has presented with. The following example should illustrate the approach: A 54-year-old male presents with a history of low back pain that radiates into his left leg. The patient works as a construction worker and has a 30-year history of smoking. Diagnostic possibilities based on the VINDICATES approach should be considered (Table 4.1).

Table 4.1 Diagnostic possibilities utilising the VINDICATES pneumonic

V=Vascular Deep vein thrombus, varicose veins, Burger’s disease, heart failure, myocardial infarction (atypical presentation), abdominal aortic aneurysm, arthrosclerosis
I=Infection Meningitis, HIV, osteomyelitis
N=Neoplastic, Neurological All carcinomas including emphasis on prostate carcinoma, lung carcinoma—Pancoast tumour, tumours of spinal cord and brain—Schwannomas, glioma, MM, Mets, osteosarcoma, Ewings sarcoma. Herniated or prolapsed vertebral disc, sciatic neuralgia, cervical spondylitic myelopathy, piriformis syndrome, cauda equine syndrome, neurogenic claudication
D=Degenerative Spondylosis of IVF, osteoarthritis, DISH
I=Inflammatory Osteomyelitis, RA, AS, EA, more arthropathie, gout
C=Cartilagenous, Congenital, Connective tissue

Pagets (as ‘bone softening’ disease), osteoporosis, scoliosis, spondylolisthesis

Duchenne muscular dystrophy and Becker’s, congenital MD

Systemic lupus erythematosus

A=Autoimmune RA, Sjögren’s , MS, SLE, AIDS T=Trauma

Fracture, → complete, stress, compression.

Whiplash syndrome.

Muscle strain, ligament sprain, e.g. lumbosacral strain-sprain

Haematoma, fibromyalgia

E=Endocrine

Hyperthyroidism, hypothyroidism, hypercalcaemia, hypocalcaemia

Hyperparathroidism, hypoparathyroidism.

Diabetes mellitus (ID and NIDDM), diabetes insipidus

Cushings, Addisons

S=Soft tissue (involvement)

Muscle strain, ligament sprain, e.g. lumbosacral strain-sprain

Haematoma, fibromyalgia, piriformis syndrome, facet syndrome, SI syndrome, torticollis, VSC, TMJ syndrome, tension/cervicogenic

Order of the history and examination process

Any healthcare practitioner with training in clinical and neural science has the ability to perform the neurological history and examination in a proficient manner. The key is to develop a routine that can easily be remembered, that can be performed in logical sequential order, and that can be easily improvised for different patient presentations. Two systematic approaches to the neurological examination include the anatomical and functional approaches. The anatomical approach requires examination of the nervous system in a rostrocaudal order (i.e. brain, brainstem/cranial nerves, spinal cord, spinal nerves, receptors, etc.), while the functional approach requires examination of related functions in groups (i.e. mental, motor, sensory, visceral, etc.). A combination of these two approaches is likely to be more efficient, less repetitive, and more appropriate for both the history-taking process and examination as well.

Greater efficiency may be achieved by limiting movement of the patient and using each tool or each type of test only once throughout the examination. If possible, the patient should be assessed in the sitting, standing, and lying positions once and should be assessed in a rostrocaudal order for each function tested. This will reduce the frequency of switching between tools and patient positions. Each instrument used in the examination should be laid out in order of use and within easy reach of the practitioner. With this orderly approach, the practitioner will be less likely to miss any component of the examination (DeMyer 1994). For example, it might be more efficient for the practitioner to determine sensitivity to pain at all levels from the ophthalmic division of the trigeminal nerve to sacral innervated regions, rather than switching between motor and sensory tests at each level.

Details gathered from the neurological history and examination may only provide information concerning the type and location of aberrant neuronal function. A thorough physical and orthopaedic examination and laboratory or ancillary neurodiagnostic tests may be more useful in establishing the aetiology in some cases.

The following lists provide an overview of the breadth of information concerning the neurological history and examination. This should serve as a useful reference and template.

The neurological history

1. Initial History

○ Onset and Character of Health Complaints
What and where are the symptoms and when did they first occur?
Was there any illness, trauma, or significant event prior to or during the onset?
What is the nature of the sensations, disabilities, or problems that have arisen?
○ Pain/Headaches/Fever/Energy or Weight Change
Has the patient experienced any pain, headaches, fever, energy, or weight change?
If weight change has occurred, was it expected from a diet or exercise programme?
○ Duration and Frequency
How long do the symptoms last and how often do they occur? Are they recurrent in nature?
○ Course
Has the patient’s condition or the symptoms changed since the onset of their condition?
○ Aggravating Factors
Is there anything that makes their symptoms worse?
○ Relieving Factors
Is there anything that makes their symptoms better?
○ Timing of Symptoms
Do the symptoms occur at a particular time of day, month, or year?
○ Treatment
Has the patient received any treatment? If so, what did it involve?
○ Sneeze/Cough/Valsalva One
Are the symptoms aggravated by pressure changes in the thorax or abdomen?
Are the symptoms affected by changes in position such as rising from a sitting or lying position?

2. General Health History

○ Family History
Have any immediate or extended family members suffered from a major or hereditary illness or expressed symptoms similar to the patient’s symptoms?
○ Accidents/Trauma
Past trauma such as motor vehicle accidents, falls, concussions, fractures, etc.
○ Medications/Supplements
Past (long-term prescriptions, etc.) or present medications.
Is the patient exposed to any other chemicals at work or home?
Is the patient taking any vitamins, remedies, or supplements?
○ Illnesses
Are there any current or past illnesses that the patient has experienced?
○ Tests and Imaging
Have any laboratory, imaging, or electrodiagnostic procedures been performed?
○ Operations/Hospitalisation
Has the patient had any surgery or admissions to hospital in the past?
○ Nutrition
What is the patient’s diet like?

3. Social History

○ Family Life
What is the patient’s marital status?
Do they have any dependants?
Do they feel much stress at home?
○ Recreation
Does the patient partake in recreational activities and exercise?
○ Education
What is their level of education?
○ Occupation
What is their job description and have there been any recent changes at work?
○ Social Drugs
Does the patient smoke or drink alcohol? If yes, how much?

4. Systems History (special senses, motor, sensory, autonomic, mental)

○ Smell and Taste
Have there been any changes to smell or taste?
Has the patient noticed any spontaneous smells or tastes?
○ Vision
Has the patient noticed any cloudiness, haziness, blurring, or double vision?
Does the patient have difficulty in stabilising their focus?
Does the patient ever experience movement of their visual environment?
Does the patient experience any pain in or around their eyes?
Is the patient more sensitive to light in one or both eyes?
○ Hearing
Has the patient ever noticed any changes to their hearing in either ear?
Does the patient find it difficult to listen when there is background noise?
Does the patient experience any ringing or whooshing noises in either ear?
Does the patient experience any pain or itchiness in or around their ears?
Does the patient experience a ‘fullness’ or ‘blocked’ sensation in either ear?
○ Balance
Does the patient find it harder to walk in a straight line?
Does the patient tend to deviate more to the left or right when walking?
Does the patient ever feel as though they are falling or leaning to one side?
Does the patient feel as though they are spinning or moving when they are still?
Does the patient ever experience any movement of their visual environment?
Has the patient experienced any nausea or vomiting?
Does the patient feel dizzy or light-headed when looking at moving objects?
Does the patient feel dizzy or light-headed when they change their posture?
○ Motor
Does the patient have any difficulty with chewing or swallowing their food?
Has the patient noticed any difficulties with speech (e.g. slurring or stuttering)?
Has the patient noticed any clumsiness (e.g. using tools and utensils, or tripping)?
Has the patient noticed any tremors or uncontrollable movements?
Has the patient noticed any stiffness, cramping, or twitching anywhere?
Has the patient noticed any weakness or wasting of muscles?
○ Sensory
Has the patient noticed any changes in skin sensitivity anywhere?
Has the patient noticed any unusual sensations anywhere (e.g. tingling, coldness)?
○ Autonomic
Has the patient noticed any changes with salivation or tearing?
Has the patient noticed any changes in sweating on either side of the body?
Has the patient noticed any coldness or puffiness in their extremities?
Does the patient feel dizzy or light-headed when they change their posture?
Does the patient experience arrhythmia or rapid changes in heart rate?
Does the patient experience any breathing difficulties?
Does the patient have any problems with digestion or bowel movements?
Does the patient suffer from ulcers or irritability in the GI tract?
Does the patient have any difficulties with initiating or controlling urination?
Has the patient experienced any signs of sexual dysfunction?
○ Mental
Have there been any changes in decision making, planning, or organisation skills?
Have there been any changes in attention levels or concentration?
Have there been any changes in behaviour, mood, or personality?
Have there been any changes in the ability to express thoughts or words?
Have there been any changes in the comprehension of speech or the written word?
Have there been any problems with the recognition of people or objects?
Have there been any changes with regard to orientation or spatial awareness?
Have there been any changes in short- or long-term memory?
Has the patient experienced any seizures, anxiety, or panic attacks?

Learning these questions as a basis for taking a neurological history can help the practitioner to gain experience by learning more about classic and unusual symptom patterns.

The neurological examination

There are numerous excellent texts that cover neurological examination techniques and these have been outlined in the Further Reading section. What will be attempted here is a description of examination techniques or procedures that either differ from the norm or are not covered in traditional texts. As each technique is encountered in the text it will be expanded on to explain in detail the approach necessary. First, some neurodiagnostic testing equipment often utilised in functional neurology will be discussed.

Neurodiagnostic tests

A variety of neurodiagnostic testing equipment can be utilised to investigate or objectively quantify dysfunction. These include:

1. Video nystagmography (VNG)—for objective analysis and documentation of visual tracking, saccade, and optokinetic dysfunction, spontaneous nystagmus with and without visual fixation, unilateral weakness (canal paresis) and directional preponderance (central asymmetry) via caloric irrigation, positional tests, and others.

2. Vestibular evoked myogenic potentials (VEMPs)—for objective analysis of certain components of the vestibulocollic reflex. Latency and amplitude of motor signals to the sternocleidomastoid (SCM) muscle are measured following stimulation of the saccule with loud auditory stimuli.

3. Balance platform—Objective analysis of postural sway in various conditions using a force platform.

4. Electrocochleography—Objective analysis of short latency responses from the cochlear apparatus and nerve.

5. Auditory brainstem responses—Objective analysis of brainstem responses to auditory stimuli to complement VEMPs.

6. Electroencephalography (EEG) and qEEG—the neuron electrical activity is measured over the scalp by very powerful receptors and then amplified to produce wave patterns that can be used to give objective projections of the state of brain function. This technique has become very powerful with the addition of source localisation software such as that offered by the Key institute which can combine low-resolution tomographic analysis (LORETA) and MRI anatomical library data to give very accurate localisation of EEG data.

7. Advanced imaging—MRI, CT, Doppler ultrasound if history and examination suggests ablative lesion of sinister aetiology or if patient is not responding to care. To be discussed further.

8. Audiometry—also useful and it is important that copies of all reports concerning hearing, vision, balance, and imaging are requested.

The examination process

Observation

1. Note the general appearance of the patient and their body morphology.

2. Note the patient’s manner and disposition.

3. Look for postural angulations of the head, trunk, and limbs.

4. Note the condition of the skin, nails, and hair.

5. Note skin lesions, pigmentary differences, nevi, oedema, and vascularity.

6. Note any asymmetries of pupil size or position, and observe for ptosis and lid lag.

7. Note any asymmetries of facial muscles and structure and observe the hairline.

Vital signs

1. Determine the heart and respiratory rate and rhythm. These signs can give an indication of the tone of the sympathetic and parasympathetic systems.

2. Determine respiratory dynamics including depth and inspiration/expiration ratio. This can give an indication of the ventilation patterns and thus the pH or acid/base state of the patient.

3. Determine blood pressure bilaterally and record even minor differences as these along with other findings can be important in determining the state of the sympathetic nervous system. Blood pressure should always be measured on both arms. Blood pressure is dependent in part on the peripheral resistance, which can be different on either side of the head and body due to asymmetrical control of vasomotor tone. Increased vasomotor tone can occur because of decreased integrity or CIS of the ipsilateral PMRF, or because of excitatory vestibulosympathetic reflexes.

4. Measure the core temperature. This may give you an indication of the basal metabolic rate of the patient, which is elevated in hyperthyroidism and some cases of infection.

5. Measure the skin and tympanic temperature bilaterally, again recording any differences as these seemingly small variations may be of great clinical importance in determining the blood flow and thus activity levels in each frontal cortex.

6. Determine oxygen saturation if the technology is available.

Visual fields and pupil responses

1. Check the upper and lower temporal and nasal visual fields. This is best done using confrontational testing procedures with a red-tipped pointer.

2. Check the patient’s pupil sizes and response to light. Both consensual and direct reflexes need to be tested and recorded.

Examination of the pupils

Pupil size reflects a balance in tone between the sympathetic and parasympathetic nervous systems. You can get a reasonable measure of the actual sympathetic tone in the patient by measuring the resting pupil size in darkness. The sympathetic tone represents the degree of dilation of the pupil but the degree of resting vascular constriction in vascular smooth muscle in most parts of the body. Vestibular, cerebellar, and cortical influences on both sympathetic and parasympathetic tone should also be considered.

Various components of the pupil light reflex are subserved by each component of the autonomic nervous system. The TTA, amplitude of constriction, smoothness and maintenance of constriction, TTF, and time to redilation of the pupil response need to be measured and recorded in each pupil. These are all aspects of the pupil light reflex that have been researched and correlated with central integrative state of the various contributing components of the nervous system.

Pupil constriction pathways

Accommodation is the constriction of the pupil that occurs during convergence of the eyes for close focusing. The Edinger–Westphal nucleus is activated by the adjacent oculomotor nucleus, which activates the medial rectus muscle more powerfully than the light reflex. There is also contraction of the ciliary muscle to aid close focusing, which is referred to as the ‘near response’. Parasympathetic fibres lie superficially on the oculomotor nerve and they relay in the ciliary ganglion of the orbit, which lies on the branch to the inferior oblique muscle. They begin in dorsal position and rotate to a medial and then inferior position as they enter the orbit. Blood supply to the pupil fibres is different from the main trunk of the nerve. The pupil fibres receive their blood supply from the overlying pia mater; therefore, the pupil fibres are usually spared in an oculomotor nerve trunk infarction.

An ‘afferent pathway lesion’ results in a Marcus-Gunn pupil. The swinging light test will reveal that the affected pupil will not react to light as well as the other pupil, but it may constrict normally in response to stimulation of the opposite pupil during testing of the consensual light reflex. This occurs in multiple sclerosis and diabetes conditions that affect the optic nerve because of demyelination or vascular lesions. One might also expect this to occur when there is an increase in sympathetic tone to the pupil on the side of relative ‘afferent’ defect. This could distinguish a high-firing IML column from TND in the mesencephalon.

The ‘Wernicke’ pupil reaction refers to differential summation depending on whether you are shining the light into the nasal or temporal aspects of the retina (i.e. intact or ablated fields). This may be observed in an optic tract lesion. Supposedly, the resting size of the pupil is uninterrupted because of the consensual light reflex. The nasal half of the retina is significantly more sensitive to light than the temporal half of the retina and the direct responses are significantly larger than the consensual response. Direct and consensual pupil reactions when stimulating the temporal retina are nearly equal. This may suggest an input of temporal retina to both sides of the pretectum. Such a crossing of temporal fibres may take place in the chiasm. The net effect of the pupillary light reaction, which involves shining light into the monocular zone from the temporal hemi-field of one eye, leads to greater constriction of the pupil on that side (Schmid et al. 2000).

Parinaud syndrome results when damage to decussating fibres of the light reflex at the level of the superior colliculus is present. This results in semi-dilated pupils fixed to light, plus loss of upward gaze.

Argyll Robertson pupil is most commonly seen in neurosyphilis: bilateral ptosis, increased frontalis tone, pupil that is irregular, small, and fixed to light, but constricts with accommodation. The pupil cannot be dilated by atropine. Differential diagnosis of this particular pupillary dysfunction includes senile miosis, pilocarpine, or β-blocker drops for glaucoma. This pattern of findings is reversed in encephalitis lethargica.

Holmes-Adie pupil or ‘tonic’ pupil occurs because of degeneration of the nerve fibres in the ciliary ganglion and is thought to be produced by a combination of slow inhibition of the sympathetic and partial reinnervation by parasympathetic fibres. This condition can also be associated with loss of patella reflex, decreased sweating, blurred vision for near work, and eye pain in bright light.

Horner’s syndrome

Disruption of the sympathetic chain at any point from the hypothalamic or supraspinal projections to the oculomotor nerve can result in a spectrum of symptoms referred to as Horner’s syndrome. The classic findings in this syndrome include ptosis, miosis, and anhidrosis but a number of other abnormalities may also be present. Ptosis or drooping of the upper eyelid is caused by the interruption of the sympathetic nerve supply to the muscles of the upper eyelid. Miosis or decreased pupil size is a result of the decreased action of the dilator muscles of the iris due to decreased sympathetic input. This results in the constrictor muscles acting in a relatively unopposed fashion, resulting in pupil constriction. A Horner’s pupil will still constrict when light is shined on the pupil although careful observation is sometimes required to detect the reduced amount of constriction that occurs. Innervation to superior and inferior tarsus muscles is carried in CN III. Vasomotor fibres are carried in the nasociliary branch of CN V and make no synapses in the ciliary ganglion after branching off from the carotid tree. Pupillodilator fibres are carried in the long ciliary branches of the nasociliary nerve.

This syndrome is characterised by the following signs and symptoms:

• Ptosis/apparent enophthalmos;

• Small pupil;

• Anhidrosis (forehead or forequarter of body);

• Bloodshot eye (loss of vasoconstrictor activity);

• Heterochromia.

Horner’s syndrome can occur because of lesions at various peripheral and central sites: hemispheric lesions, brainstem, spinal cord especially in central syringomyelia, nerve root lesions, carotid artery, jugular foramen, orbit, and cavernous sinus. Depending on the location, other cranial nerves may be involved such as III, IV, VI, and Vi near the cavernous sinus or superior orbital fissure and IX, X, and XII at the base of the skull. In the spinal cord, the mixed signs associated with syringomyelia may be present because of widening of the central canal. This would include loss of segmental reflexes, descending hypothalamospinal fibres, spinothalamic sensation (segmentally ipsilaterally and then descending contralaterally or bilaterally), ventral horn cell function, and atypical pain patterns.

With T1 nerve root involvement, Horner’s syndrome may be present with weakness of finger abduction and adduction, wasting of the intrinsic hand muscles, loss of pain sensation in the medial aspect of the arm and armpit, and deep pain in the armpit. This is rarely due to spinal degeneration, and serious causes such as Pancoast’s tumour should be considered. Referral for MRI, chest X-rays, and/or CT scan should then be considered.

Different lesion levels affect sweating differently. Central lesions may affect sweating over the entire forequarter due to involvement of the descending pathways from the hypothalamus. Lower neck lesions may affect sweating over the face only because of involvement of sympathetic efferents in the arterial plexus (carotid/vertebral). Lesions above the superior cervical ganglion may not affect sweating at all, or it may be restricted to the forehead.

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The parts of two commonly used ophthalmoscopes

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Figure 4.1 The parts of two commonly used ophthalmoscopes.

Blind spots and ophthalmoscopy

What are blind spots?

The area of the retina occupied by the nerves and blood vessels is not populated with visual receptor cells. Normally, the cells of the retinal project to the thalamus and then to the occipital cortex where their projections form ocular dominance columns, or hypercolumns. Hypercolumns represent all the possible visual characteristics of a specific point in the visual field including binocular interaction (independent ocular dominance columns), angle of perceived stimulus (orientation columns), blobs, and interblobs (colour perception units). There are a series of horizontal projecting neurons located in the visual striate cortex that allow for neighbouring hypercolumns to activate one another. The horizontal connections between these hypercolumns allow for perceptual completion to occur.

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What does it mean?

Exotropia—permanent outward deviation of one eye

Exophoria—outward deviation of one eye that corrects when the eye focuses on an object

Anisocoria—pupils of unequal size

Corectasia—dilation of the pupil

Cormyosis—constriction of the pupil

Intorsion—rotation of the eyeball towards the nose

Extorsion—rotation of the eyeball away from the nose

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Anisocoria with right corectasia

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Figure 4.2 Anisocoria with right corectasia.

The area of the visual striate cortex (occipital lobe) representing the blind spot and the monocular crescent (both in the temporal field) does not contain the alternating independent ocular dominance columns. This means that these areas only receive information from one eye. If one closes that eye, the area representing the blind spot of the eye remaining open (on the contralateral side) will not be activated because of the lack of receptor activation at the retina.

The blind spot is therefore not strictly monocular, but it is dependent on the FOF of horizontal connections from neighbouring neurons. These may be activated via receptors and pathways from either eye. Perceptual completion refers to the process whereby the brain fills in the region of the visual field that corresponds to a lack of visual receptors; therefore, we generally are not aware of the blind spot.

The size of the blind spot has been linked to the CIS of the cortex (Carrick 1997).

1. Measure the size of the patient’s blind spots using perimetry techniques (Figs 4.3 and 4.4).

a. Use a white-backed business card with a red circle drawn in one corner.
b. Stick a piece of A4 white paper on the wall or desk in landscape orientation and place a black dot in the centre that the patient can focus on.
c. Cover one of the patient’s eyes and place the patient 28 cm from the paper, ensuring that there is no head tilt present. The head should not move for the duration of the testing.
d. Move the red circle outwards from the centre and instruct the patient to inform you when the red circle disappears. Then move the circle back towards the centre until the patient informs you that the circle has returned.
e. Move the dot outwards again and repeat for eight separate points in the horizontal (2), vertical (2), and diagonal (4) planes.
f. Repeat for the other eye ensuring that the patient has not altered the position of their head.
g. Connect the dots and measure the perimetry or horizontal and vertical dimensions.
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Figure 4.3 The procedure for manual determination of blind spots.

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Figure 4.4 A blind spot map generated by a blind spot mapping computer program. The deviation of one blind spot either above or below the centre line by a significant amount can indicate a dysfunction in the optic radiations as they pass through the parietal or temporal pathways. A similar effect can be seen when the patient has tilted their head or has ocular skew when measuring the blind spots. In these cases, the deviation of the blind spots will be equidistant from the centre line. This figure demonstrates the appearance of the blind spots with a right parietal radiation dysfunction.

Blind spots can also be mapped using the Microsoft Paint program or using the computerised physiological blind spot mapper (Fig. 4.5).

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Figure 4.5 A relatively normal blind spot map generated by a blind spot map computer program. Note the volume calculations listed at the top of the figure for each blind spot. This blind spot map shows centre points that are roughly equidistant from the centre line and are thus not the result of ocular skew or head tilt.

2. Observe the anterior to posterior and nasal to temporal structures of the eye.

a. Observe the condition of the retinal vessels and determine the vein-to-artery (V:A) ratio utilising ophthalmoscopy (Fig. 4.7). Ophthalmoscopy is useful for assessing the vascularity of the optic disc and retina. This should accompany measurement of the blind spot size as changes in the morphology of the optic disc and peripapillary region of the retina could explain the shape or size of the blind spot. Changes that occur before and after an adjustment or other activity are functional in nature.

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Figure 4.7 Ophthalmoscopic appearance of the retinal arteries and veins when attempting to determine the vein-to-artery (V:A) ratio. The V:A ratio on the left is normal and on the right is increased, indicating an overactive sympathetic input to the retinal artery.

The V:A ratio refers to the difference in diameter of the veins and arteries that branch from the central retinal artery. A large difference may be due to increased sympathetic output, which causes greater peripheral resistance and constriction of arteries. The condition of blood vessels can also be helpful as an indicator of cerebrovascular integrity. Look through the ophthalmoscope and locate the vessels of the fundus. Identify a vein, which is normally larger than an artery, and an artery and then compare the sizes. The ratio of vein diameter to artery diameter can then be recorded. This is a useful procedure to perform following any intervention that may affect the sympathetic/parasympathetic activity ratio in the neuraxis.

b. Observe the fundus and look for normal appearance or any normal variants that may be present (Fig. 4.8). Observe the fundus for any pathology that may be present including vein/artery nipping, clouding or discoloration, optic nerve head swelling, subhyaloid haemorrhages, papilloedema, scarring, or melanomas (Fuller 2004) (Figs 4.9 and 4.10).
c. Nystagmus, which is a slow drift of the pupil in one direction followed by a fast correction in the opposite direction, can also be detected very easily utilising the magnification of the scope. When recording the nystagmus, it is convention to describe the direction of the fast phase as the direction of the nystagmus. For example if the pupil is seen to move slowly to the left then correct with a fast phase to the right this would be described as a right nystagmus. Nystagmus can be physiological as seen when the head is rotated or in people looking out the window of a car, peripheral, due to abnormalities of the vestibular system, central, due to cerebellar dysfunction, or retinal, due to the inability to fixate the retina on a target. Opticokinetic reflexes (OR) can be used to test visual tracking and nystagmus. Optokinetic testing can be extremely useful for determining the presence of vestibulocerebellar dysfunction and cortical hemisphericity. There is a high expectation of abnormal reflexes in patients who suffer from learning or behavioural disorders, balance problems, dizziness, vertigo, migraine, spondylosis, whiplash syndrome, anxiety, or symptoms known to be associated with cortical dysfunction (e.g. stroke).
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Figure 4.8 A normal fundus (top) and normal variants (middle and bottom) that may be observed during examination.

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Figure 4.9 The retina in a variety of retinopathies as it may be observed during examination of the fundus. These conditions, unlike the normal variants in Fig. 4.7, warrant significant medical follow-up.

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Figure 4.10 Pathologies that may be observed during examination of the fundus. These conditions, similar to those in Fig. 4.9, warrant significant medical follow-up.

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Figure 4.6 A lateral (top) and a superior (bottom) view of the correct angle of approach to start the ophthalmoscopic examination. If the patient is looking straight ahead, it also demonstrates the area of the retina that this approach should expose in the eye field of the ophthalmoscope as a point of reference for the examination. Note your viewing eye and the eye being examined in the patient should be the same, and both of your eyes should remain open during the examination.

OR can be tested by passing a opticokinetic tape in front of the patient’s eyes, first in one direction and then in the other, and observing the motion of the eyes as the tape is passed. The motion of the eyes should be observed, keeping in mind the latency and velocity of the response, the amplitude of the response, smoothness of movement of the response, the fatigability of the response, and the direction of the response, all of which should be recorded (Fig. 4.11). The opticokinetic tape can be made using a piece of white cloth about 5 cm wide and 1 m long, onto which red pieces of cloth about 5 × 5 cm2 have been stitched at regular 5-cm intervals.

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Figure 4.11 Opticokinetic tape. Saccadic eye movements, also referred to as saccades, are rapid movements that move the eye from one object to the next. The saccadic reflexes can be tested by holding an opticokinetic tape about 14 in from the eyes and moving the tape slowly and steadily first in one direction and then the other direction. Observation of the amplitude, frequency, direction, and smoothness of the saccades generated can give a clue as to the area of the neuraxis that is dysfunctional. The areas of the neuraxis largely responsible for the various phases of the slow pursuit and saccades of the eyes are highlighted in pink.

Perception of self-motion or vertigo can occur because vision-related neurons project to the medial vestibular nucleus via the nucleus of the optic tract in the pretectum.

A cortical smooth pursuit system is involved when one tries to maintain fixation of gaze on a moving object. This can be tested by slowly moving a finger from left to right in front of the patient and asking the patient to watch your finger only moving their eyes, and not their head.

Saccadic eye movements, which are also referred to as saccades, are rapid movements that move the eye from one object to the next. These can be tested by holding up fingers about 1 m apart in front of the patient and asking the patient to look from one finger to the other.

Motor examination of the head

1. Observe the orientation of the pupils and the corneal reflections. This test utilises the reflection of light off the cornea of the eyes when the patient is looking off into the distance. The reflections should be equal in size and position if the eyes are equally deviated.

2. Test the six positions of gaze and look for conjugate movements and nystagmus (Fig. 4.12). Relate the movement of the eyes to the anatomy of the eye muscles and note that the muscles of the eye will have different actions when the eye is in different positions (Fig. 4.13).

3. Observe the quality of smooth pursuit in the planes of the semicircular canals. These eye movements require activation of the cerebellum without the activation of the vestibular system and can be used to differentiate between a cerebellar and vestibular dysfunction (Fig. 4.14).

4. Palpate the jaw muscles, observe for jaw deviation, and check the jaw jerk reflex. This reflex tests the motor and sensory divisions of the mandibular division of the trigeminal nerve.

5. Observe for asymmetries in facial muscle contraction, both voluntary and involuntary actions, and both upper and lower face need to be tested. The CN VII nucleus is innervated bilaterally by upper motor corticobulbar neurons. The CN VII nerve itself is ipsilateral in projection to the face. This results in a situation where damage to the CN VII nerve (lower motor neuron) results in ipsilateral paralysis involving the whole side of the face. When supranuclear damage (upper motor neuron) is present, the paralysis is limited to the contralateral forehead area (Fig. 4.15).

6. Observe for asymmetry in palate elevation (Fig. 4.16).

7. Observe for fasciculations, atrophy, and deviation of the tongue.

8. Observe and feel the tone of the SCM and trapezius muscles during head turning.

9. Observe the quality of the ocular tilt reaction. The OTR is a reflex movement of the eyeball when the head is tilted from one side to the other. When the head tilts to the right the right eye should intort (roll towards the nose) and the left eye should extort (roll away from the nose). This is a vestibular ocular reflex.

10. Observe the patient’s optokinetic reflexes (see above).

11. Observe the patient’s saccades and anti-saccades (see above).

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Figure 4.12 Movement directions produced by contractions of the extraocular muscles. The directions outlined represent the primary direction of movement of each muscle when the eyeball is facing forward in a neutral gaze and with no synergic activity of other extraocular muscles involved. SR, superior rectus; IR, inferior rectus; IO, inferior oblique; SO, superior oblique; LR, lateral rectus; MR, medial rectus.

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Figure 4.13 Superior view of the extraocular muscles of the right eye. Note the origin and insertion of the muscles with respect to the midline of the eyeball.

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Figure 4.14 Eye movements and their related vestibular canals stimulated when these eye movements are accompanied by a rotation of the head in order to focus on a moving object or keep an object in focus while the head is moving.

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Figure 4.15 Innervation of the facial muscles by the facial nerve (CN VII). The corticobulbar projections (1) arise from the cortical facial areas and project to the facial nerve nuclei. These projections are bilateral from the cortex to the areas of the facial nucleus supplying the upper eyelid and forehead and contralateral to the nuclei supplying the lower face. The projections of the cranial nerve nuclear neurons form the facial nerve (CN VII) proper and project ipsilateral to the upper and lower face (2). Thus, a facial nerve (CN VII) lesion, also referred to as a lower motor neuron lesion, will result in paralysis of the ipsilateral facial muscles of both the upper and lower face. A lesion to the cortical areas or the corticobulbar projection pathways, also referred to as an upper motor neuron lesion, will result in a contralateral facial paralysis of the lower face only.

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Figure 4.16 View of the mouth and palate during examination. (Top) Normal palatal elevation and (bottom); left palatal paresis. The latter may be due to a number of reasons including muscular weakness, glossopharyngeal nuclear dysfunction, and decreased neural stimulus from the ipsilateral corticobulbar neurons. Note the uvula rarely deviates in this condition as opposed to the complete paralysis of the glossopharyngeal nerve where it deviates away from the side of the lesion.

Sensory examination of the head

1. Check sensation to pinprick (or pinwheel) in trigeminal and cervical zones (Fig. 4.17).

2. Check sensation to light touch, if indicated.

3. Check for quality and asymmetry of the corneal reflex. Many students and practitioners get false results from this reflex because of faulty technique. Several common mistakes include touching the conjunctiva instead of the cornea, approaching the eye too quickly, which is perceived as menacing and results in a blink reflex, and testing over a contact lens, all of which result in inaccurate findings. The area of the eye touched to trigger this reflex correctly is shown in Figure 4.18. The reflex is performed by asking the patient to look up and away and slowly bring a piece of cotton wool twisted to a point in contact with the cornea. Watch for the reaction of both eyes, and the ocular muscles surrounding the eye. The normal response is a bilateral blink and contracture of the muscles of the eyebrows bilaterally. If there is failure of either side to blink you can suspect an ipsilateral trigeminal nerve (CN V) V1 lesion on the side you are testing. If only one side fails to respond you could expect a facial (CN VII) lesion on the side that fails to contract.

4. Perform gag reflex if indicated.

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Figure 4.17 (A) Actual nerve pathways of the face and head. (B) Dermatomal distribution of the receptive fields of the nerves of the head and face. Note that the trigeminal nerve’s occipital division has a dermatomal distribution that projects from the tip of the nose to well past the ears on the top of the head and the mandibular division projects anterior to the ear to cover the temporal area.

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Figure 4.18 The corneal reflex.

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Commonly presenting movement disorders

• Essential tremor

• Parkinson’s disease

• Dystonia

• Spasmodic torticollis

• Writer’s cramp

• Primary dystonia of essential tremor

• Restless leg syndrome

• Spasmodic dysphonia

• Meige’s syndrome

Taste, smell, hearing, and otoscopic inspection

1. Check taste sensation on each side of the tongue.

2. Test for smell sensation in each nostril.

3. Check hearing with Weber’s, Rinne’s, and other tests if necessary.

4. Perform otoscopic inspection. This is useful for observing the integrity of the tympanic membrane and investigating the presence of middle and outer ear abnormalities including wax accumulation. History of ear infection may provide an insight into the aetiology of vestibular and auditory symptoms.

Cranial nerve screening

The majority of signs and symptoms associated with brainstem dysfunction can be revealed by performing a thorough history and examination of the cranial nerves and their effects on sensory, motor, autonomic, and mental functions. The list below includes motor, sensory, and autonomic signs observed at both cranial and spinal levels that may be mediated by the various cranial nerves and neighbouring reticular formation.

CN I Olfactory

1. Smell in independent nostrils

CN II Optic

1. Pupil size

2. Pupil light reflexes

3. Light sensitivity—vestibular-induced increase contralaterally

4. Blind spot size and orientation

5. Acuity

6. Visual fields

An upper temporal field deficit may be found in the contralateral eye to an optic nerve lesion because of looping of the contralateral lower nasal retinal fibres back along the optic nerve.

Incongruous field defects can occur because of involvement of the optic tracts between the optic chiasm and the lateral geniculate nucleus (LGN) (thalamus) and midbrain. This is due to the 90° inward rotation of the tracts so that both sets of lower field fibres lie medially, and both sets of upper field fibres from each eye lie laterally.

CN III Oculomotor

1. Corneal reflection abnormalities

2. Weakness on gaze

3. Nystagmus—vestibular-induced slow phase contralaterally

4. Opticokinetic reflexes (OPK)—slower contralateral to deficit

5. Saccades/pursuits—dysmetric contralaterally

6. OTR

7. Blepharospasm—vestibular-induced enhancement of blink reflex

CN IV Trochlear

1. Corneal reflection abnormalities

2. Weakness on gaze

3. Nystagmus

4. OKN

5. Saccades/pursuits

6. OTR

CN V Trigeminal

1. Masticator tone—vestibular-induced increase (esp. contralaterally)

2. Sensation—vestibular-induced disinhibition of pain

3. Ear pain

4. Corneal reflex (afferent limb)—vestibular/anxiety-induced enhancement

CN VI Abducens

1. Corneal reflection abnormalities

2. Weakness on gaze

3. Nystagmus

4. OKN

5. Saccades/pursuits

CN VII Facial

1. Facial tics—peripheral or basal ganglionic mechanisms

2. Ear pain

3. Salivation—vestibular-induced increase due to PMRF integration (superior salivatory nucleus)

CN VIII Vestibular and Cochlear

1. OTR

a. Skew deviation
b. Ocular torsion
c. Head tilt
d. Subjective visual vertical (SVV)—cortical consequences

2. Corneal reflection abnormalities

3. Weakness on gaze—contralateral to deficit

4. Nystagmus—vestibular-induced slow phase contralaterally

5. OKN

a. Slower pursuit contralateral to deficit
b. Dysmetric pursuit contralateral to hyper- or hypofunction

6. Saccades/pursuits—as above

7. Vestibulo-ocular reflexes (VORs)—decreased gain with rotation to side of deficit

8. Vestibulo-autonomic reflexes as above and below (heart, lungs, gut, head)

9. Neck muscle tension and pain—vestibular-induced increase

10. Extensor muscle tone—vestibular-induced increase

11. Somatic sensation—vestibular-induced pain, ‘numbness’, tingling, etc.

12. Motor and sensory trigeminal signs as above (5)

13. Light sensitivity—vestibular-induced increase contralaterally

14. Postural head tilt—most commonly to side of deficit

15. Deviation on Romberg’s test or walking—most commonly to side of deficit

16. Increased postural sway in sagittal or coronal planes

17. Rotation or side-stepping on Fukuda’s test (marching on the spot with eyes closed for 30 s)—most commonly to side of deficit

18. Accompanying hearing deficits and tinnitus—peripheral mechanisms

19. Hearing deficits and/or tinnitus—altered autonomic and/or dorsal cochlear nucleus integration

20. Aural fullness—sensation of fullness or pain in the ear or surrounding head

21. Frequent headaches (occipital to frontal)—aggravated by fatigue, visual work, light, oversleeping

CN IX Glossopharyngeal

1. Baroreceptor reflexes—interaction with vestibulosympathetic reflexes

2. Ear pain

3. Salivation—vestibular-induced increase due to PMRF integration (inferior salivatory nucleus)

CN X Vagus

1. Difficulty or tightness swallowing—vestibular-induced anxiety syndrome

2. Increased or decreased bowel movements/sounds (auscultation)—vestibular-induced activation of DMN X

3. Bradycardia—depending on interaction with vestibulosympathetic reflexes (vestibular-induced activation of nucleus ambiguus)

4. Nausea—activation of NTS, DMN X, and emetic centres

5. Ear pain

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Frequently observed in patients with chronic vestibulocerebellar disorders

• General Dystonias

• Writer’s cramp
• Causalgic-dystonia (reflex sympathetic dystrophy (RSD), repetitive strain, chronic pain, etc.)

• Facial Tics

• Peripheral nerve lesion (see slides on blepharospasm)
• Vestibular disorders
• Mood disorders—anxiety, panic, and obsessive-compulsive disorder (OCD)
• Dystonic

• Restless Leg Syndrome

• Akathisia

• Essential Tremor

• Vestibular and cerebellar dysfunction (inner ear disease)

• Parkinsonism

• Mood disorders
• Medications

CN XI Spinal Accessory

1. Postural deviations of head—most commonly tilted to side of deficit (there are other important factors such as increased posterior muscle tone)

CN XII Hypoglossal

1. Tongue muscle tone—vestibular-induced increase

Motor examination of the trunk and limbs

1. Check upper and lower limb muscles for segmental or suprasegmental weakness (see muscle testing diagrams at Figs 4.21 to 4.31).

2. Check upper and lower limb reflexes (see Fig. 4.32). Reflexes should be tested by applying repeated equal strikes of the reflex hammer to the tendon until fatigue occurs or until six or seven strikes have been performed. If the muscle maintains equal responses throughout the six or seven repeated stimuli then the area supplying that reflex can be thought of as expressing a healthy CIS.

3. Check the resistance in muscles to joint motion (muscle tone).

4. Assess for percussion irritability and myotonia.

5. Check flexor reflex afferent reflexes, which include the superficial abdominal and plantar reflexes. The superficial abdominal reflex is performed by scratching the abdominal wall as shown in Figure 4.19 and observing the reaction of the abdominal muscles, which should contract on the same side. The afferent supply for this reflex is thought to be the segmental sensory nerves and the efferent supply the segmental motor nerves. The roots tested when striking above the umbilicus are T8–T9 and below the umbilicus T10 and T11. No reaction of the abdominal muscles is a positive response and is thought to indicate an upper motor neuron lesion at the level being tested, but may also present if the lower motor neuron is involved. However, this test is not accurate in a large number of individuals because of the presence of large amounts of abdominal fat or scar tissue formation, or in women who have experienced multiple pregnancies.

6. The plantar reflex or response (Fig. 4.20) is performed by stroking the plantar aspect of the foot, making sure to curve under the area where the toes join the foot. A normal response involves the toes curling downwards and a mild jerk of the foot away from the stimulus. A positive response, also known as a Babinski response, involves the upward movement of the toes, and in some cases only the big toe moves upwards, which is referred to as an up-going toe. A positive response indicates a lesion to the corticospinal tract on the ipsilateral side below the decussation of the fibres in the medulla, or a contralateral lesion of the corticospinal tracts above the decussation. Commonly, this type of neuron injury is referred to as an upper motor neuron lesion.

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Figure 4.21 (A) Trapezius, upper portion (C3, 4; spinal accessory nerve). The shoulder is elevated against resistance. (B) Trapezius, upper portion (C3, 4; spinal accessory nerve). The shoulder is thrust backward against resistance.

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Figure 4.22 (A) Rhomboids (C4, 5; dorsal scapulary nerve). The shoulder is thrust backward against resistance. (B) Serratus anterior (C5–7; long thoracic nerve). The subject pushes hard with outstretched arms; the inner edge of the scapula remains against the thoracic wall. (If the trapezius is weak, the inner edge may move from chest wall.) (C) Infraspinatus (C4–6; suprascapular nerve). With the elbow flexed at the side, the arm is externally rotated against resistance on the forearm. (D) Supraspinatus (C4–6; suprascapular nerve). The arm is abducted from the side of the body against resistance.

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Figure 4.23 (A) Latissimus dorsi (C6–8; subscapular nerve). The arm is abducted from a horizontal and lateral position against resistance. (B) Deltoid (C5, 6; axillary nerve). Abduction of laterally raised arm (30°–75° from body) against resistance. (C) Pectoralis major, upper portion (C5–8; lateral and medial pectoral nerves). The arm is abducted from an elevated or horizontal and forward position against resistance. (D) Pectoralis major, lower portion (C5–8, T1; lateral and medial pectoral nerves). The arm is abducted from forward position below horizontal against resistance.

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Figure 4.24 (A) Biceps (C5, 6; musculocutaneous nerve). The supinated forearm is flexed against resistance. (B) Triceps (C6–8; radial nerve). The forearm, flexed at the elbow, is extended against resistance. (C) Brachioradialis (C5, 6; radial nerve). The forearm is flexed against resistance while it is in ‘neutral’ position (neither pronated nor supinated). (D) Extensor digitorum (C7, 8; radial nerve). The fingers are extended at the metacarpophalangeal joints against resistance. (E) Supinator (C5, 6; radial nerve). The hand is supinated against resistance, with arms extended at the side. Resistance is applied by the grip of the examiner’s hand on patient’s forearm near the wrist.

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Figure 4.25 (A) Extensor carpi radialis longus (C6–8; radial nerve). The wrist is extended to the radial side against resistance; fingers extended. (B) Extensor carpi ulnaris (C6–8; radial nerve). The wrist joint is extended to the ulnar side against resistance. (C) Extensor pollicis longus (C7, 8; radial nerve). The thumb is extended against resistance. (D) Extensor pollicis brevis (C7, 8; radial nerve). The thumb is extended at the metacarpophalangeal joint against resistance. (E) Extensor indicis proprius (C6–8; radial nerve). The index finger is extended against resistance placed on the dorsal aspect of the finger. (F) Abductor pollicis longus (C7, 8, T1; radial nerve). The thumb is abducted against resistance in a plane at right angle to the palmar surface.

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Figure 4.26 (A) Flexor carpi radialis (C6, 7; median nerve). The wrist is flexed to the radial side against resistance. (B) Flexor digitorum sublimis (C7, 8, T1; median nerve). Fingers are flexed at first interphalangeal against resistance; proximal phalanges fixed. (C) Flexor digitorum profundus I and II (C7, 8, T1; median nerve). The terminal phalanges of the index and middle fingers are flexed against resistance, the second phalanges being held in extension. (D) Pronator teres (C6, 7; median nerve). The extended arm is pronated against resistance. Resistance is applied by grip of examiner’s hand on patient’s forearm near the wrist. (E) Abductor pollicis brevis (C7, 8, T1; median nerve). The thumb is abducted against resistance in a plane at a right angle to the palmar surface.

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Figure 4.27 (A) Flexor pollicis longus (C7, 8, T1; median nerve). The terminal phalanx of the thumb is flexed against resistance as the proximal phalanx is held in extension. (B) Flexor pollicis brevis (C7, 8, T1; median nerve). The proximal phalanx of the thumb is flexed against resistance placed on its palmar surface. (C) Opponens pollicis (C8, T1; median nerve). The thumb is crossed over the palm against resistance to touch the top of the little finger with the thumbnail held parallel to the palm. (D) Lumbricalis-interossei (radial half) (C8, T1; median and ulnar nerves). The second and third phalanges are extended against resistance; the first phalanx is in full extension. The ulnar has the same innervation and can be tested in the same manner. (E) Flexor carpi ulnaris (C7, 8, T1; ulnar nerve). The little finger is abducted strongly against resistance as the supinated hand lies with fingers extended on table. (F) Flexor digiti quinti (C7, 8, T1; ulnar nerve). The proximal phalanx of the little finger is flexed against resistance.

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Figure 4.28 (A) Flexor digitorum profundus III and IV (C8, T1; ulnar nerve). The distal phalanges of the little and ring fingers are flexed against resistance; the second phalanges are held in extension. (B) Abductor digiti quinti (C8, T1; ulnar nerve). The little finger is abducted against resistance as the supinated hand with fingers extended lies on table. (C) Opponens digiti quinti (C7, 8, T1; median nerve). With fingers extended, the little finger is moved across the palm to the base of the thumb. (D) Abductor pollicis (C8, T1; ulnar nerve). A piece of paper grasped between the palm and the thumb is held against resistance with the thumbnail kept at a right angle to the palm. (E) Dorsal interossei (C8, T1; ulnar nerve). The index and ring fingers are abducted from midline against resistance as the palm of the hand lies flat on the table. (F) Palmer interossei (C8, T1; ulnar nerve). The abducted index, ring, and little fingers are adducted to midline against resistance as the palm of the hand lies flat on the table.

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Figure 4.29 (A) Sartorius (L2, 3; femoral nerve). With the subject sitting and the knee flexed, the thigh is rotated outward against resistance on the leg. (B) Quadriceps femoris (L2–4; femoral nerve). The knee is extended against resistance on the leg. (C) Iliopsoas (L1–3; femoral nerve). The subject lies supine with knee flexed. The flexed thigh (at about 90°) is further flexed against resistance. (D) Adductors (L2–4; obturator nerve). With the subject on one side with knees extended, the lower extremity is adducted against resistance; the upper leg is supported by the examiner. (E) Gluteus medius and minimus; tensor fasciae latae (L4, 5, S1; superior gluteal nerve). Testing abduction: With the subject lying on one side and the thigh and leg extended, the uppermost lower extremity is abducted against resistance.

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Figure 4.30 (A) Gluteus medius and minimus; tensor fasciae latae (L4, 5, S1; superior gluteal nerve). Testing internal rotation: With the subject prone and the knee flexed, the foot is moved laterally against resistance. (B) Gluteus maximus (L4, 5, S1, 2; inferior gluteal nerve). With the subject prone, the knee is lifted off the table against resistance. (C) ‘Hamstring’ group (L4, 5, S1, 2; sciatic nerve). With the subject prone, the knee is flexed against resistance. (D) Gastrocnemius (L5, S1, 2; tibial nerve). With the subject prone, the foot is plantar-flexed against resistance. (E) Flexor digitorum longus (S1, 2; tibial nerve). The toe joints are plantar-flexed against resistance.

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Figure 4.31 (A) Flexor hallucis longus (L5, S1, 2; tibial nerve). The great toe is plantar-flexed against resistance. The second and third toes are also flexed. (B) Extensor hallucis longus (L4, 5, S1; deep peroneal nerve). The large toe is dorsiflexed against resistance. (C) Extensor digitorum longus (L4, 5, S1; deep peroneal nerve). The toes are dorsiflexed against resistance. (D) Tibialis anterior (L4, 5; deep peroneal nerve). The foot is dorsiflexed and inverted against resistance applied by gripping the foot with the examiner’s hand. (E) Peroneus longus and brevis (L5, S1; superficial peroneal nerve). The foot is everted against resistance applied by gripping the foot with the examiner’s hand. (F) Tibialis posterior (L5, S1; tibial nerve). The plantar-flexed foot is inverted against resistance applied by gripping the foot with the examiner’s hand.

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Figure 4.32 (A) Testing the biceps reflex; (B) testing the supinator reflex; (C) testing the triceps reflex; (D) testing the knee reflex; (E) the ankle reflex and three ways to get it.

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Figure 4.19 The superficial abdominal reflex is performed by scratching the abdominal wall as shown and observing the reaction of the abdominal muscles, which should contract on the same side.

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Figure 4.20 The plantar reflex or response is performed by stroking the plantar aspect of the foot with a blunted sharp edge such as the pointed end of the reflex hammer.

image Quick facts 4.12

The following points are central to the initial assessment of a movement disorder

1. Determine the characteristics of the movement.

2. Determine the likelihood of heredity.

3. Enquire about inciting events and exposures to drugs/toxins, etc.

4. Determine the time course of the disorder.

5. Investigate for coexisting medical or neurological disease.

Sensory examination of the trunk and limbs

1. Check spinothalamic sensation, which includes pain and temperature in upper and lower limbs. A common mistake made when performing this test is to be too gentle and not actually cause pain. The patient may respond that they felt the stimulus but the stimulus they felt was not pain but pressure. If you are testing pain then it must cause pain to test it.

2. Check dorsal column sensation, which includes two-point discrimination and vibration sense, in upper and lower limbs. A good way to check vibration sense is to use a low C tuning fork, set it ringing, and apply the single pronged end to a distal point on the fingers or toes.

3. Determine presence of:

a. Astereognosis, which is the inability to identify a common object when placed in the hand with eyes closed
b. Atopognosia, which is the inability to correctly localise a sensation and
c. Graphanaesthesia which is the failure to recognise a number drawn on the patient’s palm which is not in view of the patient.

Cerebellar (and further vestibular) examination

1. Observe for the presence of a resting, postural, or kinetic tremor.

a. Check all limbs for past pointing/overshooting, by asking the patient to extend their arms out to each side with their first finger extended and touch the fingers in alternating fashion to their nose. Do this first with eyes open and then with eyes closed. To test the lower limbs have them run the heel of one foot down the shin of the opposite leg to the toes.

image Quick facts 4.13

Testing for cerebellar dysfunction

• Walk in tandem, on heels, on toes, and backwards
• Accentuate dysmetria by increasing inertial load of limb (overshooting and undershooting)
• Finger opposition, pronation, and supination of the elbow, heel/toe floor tapping (disdiadochokinesia)
• Finger to nose, toe to finger, heel to shin, figure-of-eight (kinetic tremor and dysmetria)
• Rotated postures of the head.

image Quick facts 4.14

Not to be missed tests in all cases of suspected vestibular and auditory dysfunction

1. Cranial nerve screen
2. Corneal reflexes
3. Trigeminal sensation (especially first division)
4. Plantar reflexes
5. Basic motor and sensory examination
6. Cerebellar screening.

b. Dysmetria—check all movements for smoothness and accuracy of performance.
c. Disdiadochokinesia is present if the patient cannot perform rapid alternating movements in a consistent, symmetrical, and coordinated fashion. A good test is to ask the patient to rapidly turn both of their hands from palm up to palm down as rapidly as they can and compare the actions of each hand.

2. Instruct the patient to walk on their toes and heels and perform tandem gait.

3. Perform:

a. Romberg’s test, which is testing the posterior columns and cerebellum. Ask the patient to stand with their feet close together or touching. Then ask them to raise their arms to shoulder height and keep them extended in space at the same height. Observe the degree to which they sway. If the sway is not to such an extent that they may fall, ask them to close their eyes and again observe the sway. Watch very closely for the direction of movement or any preferences in direction that they like to move into. Have them maintain this posture for approximately 30 s. Then ask them to open their eyes and tell you what they felt. Patients will usually fall to the side of decreased cortical muscle tone or the side of increased cerebellar activation.
b. Fukuda’s marching in place test, which is performed by asking the patient to march on the spot, lifting their right arm and leg in unison and likewise for the left arm and leg. Have them complete the cycle a few times and then ask them to close their eyes. Keep them marching for about 30 s and note any deviation from the spot that they started on.

image Quick facts 4.15

Frontal lobe testing

• Clinical tests

• Digit span (forwards and backwards)

• Motor strength and tone

• Limb control

• Blink rates

• Glabellar tap test (e.g. depression, mania, Parkinson’s, dementia)

• Other release phenomena

• Spontaneous lateral eye movements

• Saccade accuracy

• Anti-saccades

• Remembered saccades

• Forehead skin temperature

• Tympanic temperature

Orthopaedic examination

Check both passive and active range of motion of all joints including the extremities. Check muscle strength (see muscle testing diagrams at the end of this chapter). Observe the patient’s gait and posture.

Physical (visceral) examination

1. Chest—not covered in this text.

a. Heart: Tachycardia or arrhythmia—due to IML escape (especially on the right and left respectively as the right IML has greater control of the sinoatrial node, while the left IML has greater control of the atrioventricular node). This may occur because of decreased integrity of the PMRF or increased expression of vestibulosympathetic reflexes. Arrhythmias and changes in heart sounds can occur due to altered CIS of the PMRF.
b. Lungs—not covered in this text

2. Abdominal exam—not covered in this text.

Examination of mental state

The patient should be tested for orientation to person: Do they know who they are? place—Do they know where they are? and time—Do they know what day, month, and year it is? One should also test for both short- and medium-term memory by asking the patient to remember a six-digit number and repeat it back immediately and then again after a few minutes have passed and they have been distracted by other testing.

We have now covered some background information about neuron theory, functional neuroanatomy, and the objectives of performing a functional neurological examination. The focus in the following will now be on determining the presence of dysfunction and asymmetry as part of the wider functional neurological examination.

1. Vestibulocerebellar system

2. Autonomic system

3. Cerebral neuronal activity—hemisphericity.

Vestibulocerebellar dysfunction and asymmetry

The SEE principle (Spine, Ears, and Eyes)

There is substantial integration of spine, ear, and eye afferents at numerous levels of the neuraxis. The four major areas involved in this multimodal integration include the following:

1. Vestibulocerebellar system

2. Mesencephalon

3. Pulvinar and posterior thalamic nuclei and

4. Parietotemporal association cortex.

Integration in all regions may affect the CIS of the IML column and autonomic nuclei in the brainstem. However, convergence of spine, ear, and eye afferents in the vestibulocerebellar system and mesencephalon will have a more direct affect and the relationship between dysfunction in these areas and autonomic asymmetry can be readily observed.

Signs and symptoms of vestibulocerebellar dysfunction may be associated with increased or decreased vestibular output, referred to below as ‘vestibular-induced’ and ‘deficit-induced’, respectively. Despite these delineations, a vestibular-induced symptom may, in fact, be due to vestibular hypofunction on the contralateral side and vice versa. Dysmetric eye movements and some signs associated with autonomic function are not classed as being due to hypo- or hyperfunction, as individual bedside tests may not be adequate to confirm this relationship. All clinical signs and symptoms help to establish the diagnosis or clinical impression.

The following aspects need to be considered when determining the presence of vestibulocerebellar dysfunction:

• Vestibulosympathetic reflexes

• Vestibular/fastigial connections to the PMRF

• Motor consequences

• Sensory consequences and

• Mental consequences.

Extraocular movements

1. Dorsal vermis

○ Saccadic dysmetria (hypermetric) and macrosaccadic oscillations
○ Pursuit
○ Saccadic lateropulsion

2. Flocculus and paraflocculus Gaze-evoked nystagmus

○ Rebound nystagmus
○ Downbeat nystagmus
○ Smooth tracking
○ Glissadic, postsaccadic drift
○ Disturbance in adjusting the gain of the VOR

3. Nodulus Increase in duration of vestibular response

○ Periodic alternating nystagmus.

Autonomic dysfunction and asymmetry

What components of the neurological, physical, or orthopaedic examinations allows one to gain some information about autonomic function?

1. Width of palpebral fissure (ptosis)—This is dependent on both sympathetic and oculomotor innervation. Therefore, one needs to differentiate between a Horner’s syndrome, oculomotor nerve lesion, or physiological changes in the CIS of the mesencephalic reticular formation.

2. Skin condition—Increased peripheral resistance may result in decreased integrity of skin, particularly at the extremities.

3. Ophthalmoscopy—V:A ratio and vessel integrity.

4. Heart auscultation—Arrhythmias and changes in heart sounds can occur because of altered CIS of the PMRF.

5. Bowel auscultation—This can be particularly useful during some treatment procedures to monitor the effect of stimulation on vagal function (e.g. caloric irrigation—further instruction required, adjustments and visual stimulation or exercises, etc.).

6. Skin and tympanic temperature and blood flow—This is particularly useful as a pre- and post-adjustment check. Profound changes in skin temperature asymmetry can occur following an adjustment. These changes are side dependent. An adjustment on the side of decreased forehead skin temperature will commonly result in greater symmetry or reversed asymmetry. Conflicting results are likely to be dependent on a number of factors, which are currently being investigated further. Remember that forehead skin temperature depends on fuel requirements of the brain, and vestibular and cortical influences on autonomic function, among other things.

7. Dermatographia—The red response is often observed in patients who suffer from sympathetically mediated pain.

8. Lung expansion, respiratory rate and ratio, etc.—An inspiration:expiration ratio of 1:2 is considered to represent approximately normal sympathovagal balance. This means that expiration should take twice as long as inspiration. This is difficult to achieve for some patients at first and requires some training.

Shallow and rapid breathing can result in respiratory alkalosis, which leads to hypersensitivity in the nervous system. CO2 is blown off at a higher rate, resulting in decreased [H+] ions in the blood. Lower [Ca++] follows, causing [Na+] to rise in extracellular fluid. This can be seen clinically by the presence of percussion myotonia, which is also often seen in various metabolic and hormonal disorders.

9. Forehead skin temperature—Measurement of skin temperature above the browline may provide useful information concerning sympathetic control of blood vessels to the eye, as sympathetic supply to the vessels of the forehead are branches of the sympathetic supply to the retinal vessels. Activation of cervical afferents has been found to have an antagonistic effect on the excitatory vestibulosympathetic reflexes. It is therefore proposed that a cervical spine adjustment may enhance cervical inhibition of the vestibulosympathetic reflex, resulting in increased blood flow to the eye and brain (Sexton 2006).

Motor examination of the trunk and limbs

Table 4.2 Muscle innervation listed by individual nerves

Upper extremity Lower extremity

Suprascapular nerve

Shoulder girdle
Supraspinatus
Infraspinatus

Superior gluteal nerve

Buttock
Gluteus medius
Gluteus minimus
Tensor fasciae latae

Long thoracic nerve

Shoulder girdle
Serratus anterior

Inferior gluteal nerve

Buttock
Gluteus maximus

Axillary nerve

Shoulder girdle
Teres minor
Deltoid

Femoral nerve

Thigh
Pectineus
Sartorius
Quadriceps femoris (rectus femoris, vastus lateralis, vastus intermedius, vastus medialis)

Musculocutaneous nerve

Arm
Biceps brachii
Coracobrachialis
Brachialis

Obturator nerve

Thigh
Adductor longus
Gracilis
Adductor brevis
Obturator externus
Adductor magnus

Median nerve

Forearm
Pronator teres
Flexor carpi radialis
Palmaris longus
Flexor digitorum sublimes
Flexor pollicis longus
Pronator quadratus
Hand
Abductor pollicis brevis
Opponens pollicis
Flexor pollicis brevis
Lumbricales I and II

Sciatic nerve, tibial division

Thigh
Semitendinosus
Biceps (long head)
Semimembranosus
Popliteal space (tibial nerve)
Gastrocnemius
Plantaris
Popliteus
Soleus
Leg
Tibialis posterior
Flexor digitorum longus
Flexor hallucis longus
Foot
Abductor hallucis
Abductor digiti minimi
Dorsal interossei

Radial nerve

Arm
Triceps (long head, lateral head, medial head)
Anconeus
Brachioradialis
Extensor carpi radialis
Forearm
Extensor carpi radialis brevis
Supinator longus
Extensor digitorum communis
Extensor digit quinti
Extensor carpi ulnaris
Abductor pollicis longus
Extensor pollicis brevis
Extensor indicis proprius

Sciatic nerve, peroneal division

Thigh
Biceps (short head)
Leg (deep peroneal nerve)
Tibialis anterior
Extensor hallucis longus
Extensor digitorum longus
Peroneus tertius
Foot
Extensor digitorum brevis
Leg (superficial peroneal nerve)
Peroneus longus
Peroneus brevis

Ulnar nerve

Forearm
Flexor carpi ulnaris
Flexor digitorum profundus (medial half)
Hand
Flexor digiti quinti brevis
Abductor digiti quinti
Oppenens digiti quinti
Interossei
Lumbricales III and IV
Adductor pollicis
Flexor pollicis brevis (deep part)
 

From Chusid 1964 with permission.

Table 4.3 Motor function chart

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image Clinical case answers

Case 4.1

4.1.1

You would need to examine CN III, V, VII, IX, and X. The examinations one would perform are:

1. Width of palpebral fissure (ptosis)—This is dependent on both sympathetic and oculomotor innervation. Therefore, one needs to differentiate between a Horner’s syndrome, oculomotor nerve lesion, or physiological changes in the CIS of the mesencephalic reticular formation.

2. Skin condition—Increased peripheral resistance may result in decreased integrity of skin, particularly at the extremities.

3. Ophthalmoscopy—V:A ratio and vessel integrity.

4. Heart auscultation—Arrhythmias and changes in heart sounds can occur because of altered CIS of the PMRF.

5. Bowel auscultation—This can be particularly useful during some treatment procedures to monitor the effect of stimulation on vagal function (e.g. caloric irrigation—further instruction required, adjustments and visual stimulation or exercises, etc.).

6. Skin and tympanic temperature and blood flow—This is particularly useful as a pre- and post-adjustment check. Profound changes in skin temperature asymmetry can occur following an adjustment. These changes are side dependent. An adjustment on the side of decreased forehead skin temperature will commonly result in greater symmetry or reversed asymmetry. Conflicting results are likely to be dependent on a number of factors, which are currently being investigated further. Remember that forehead skin temperature depends on fuel requirements of the brain, and vestibular and cortical influences on autonomic function among other things.

7. Dermatographia—The red response is often observed in patients who suffer from sympathetically mediated pain.

8. Lung expansion, respiratory rate and ratio, etc.—An inspiration:expiration ratio of 1:2 is considered to represent approximately normal sympathovagal balance. This means that expiration should take twice as long as inspiration. This is difficult to achieve for some patients at first and requires some training. Shallow and rapid breathing can result in respiratory alkalosis, which leads to hypersensitivity in the nervous system. CO2 is blown off at a higher rate, resulting in decreased [H+] ions in the blood. Lower [Ca++] follows, causing [Na+] to rise in extracellular fluid. This can be seen clinically by the presence of percussion myotonia, which is also often seen in various metabolic and hormonal disorders.

9. Forehead skin temperature—Measurement of skin temperature above the browline may provide useful information concerning sympathetic control of blood vessels to the eye, as sympathetic supply to the vessels of the forehead are branches of the sympathetic supply to the retinal vessels. Activation of cervical afferents has been found to have an antagonistic effect on the excitatory vestibulosympathetic reflexes. It is therefore proposed that a cervical spine adjustment may enhance cervical inhibition of the vestibulosympathetic reflex, resulting in increased blood flow to the eye and brain.

4.1.2

1. Pupil size and reactivity

2. Retinal artery V:A ratios

3. Bilateral blood pressure

4. Skin temperature and sweat production

5. Presence of dermatographia

6. Heart rate

4.1.3

Dermatographia is an exaggerated wheal and flare response to lines drawn on the skin with a pointed but blunt instrument. It is also referred to as the red response. The red response is often observed in patients who suffer from an overactive sympathetic nervous system or sympathetically mediated pain.

Case 4.2

4.2.1

Exotropia is the deviation of the eye away from the nose when the eye is stationary but the degree of deviation usually remains no matter how the eye is moved. It is a form of strabismus (Fig. 4.2.1). Exophoria is a mild deviation of the eye towards the nose during movement of the eye that is normally not detected by the individual because integration in the brain can accommodate the minor variance. Both may be caused by a weak medial rectus muscle or an overactive lateral rectus muscle.

4.2.2

The activity level of both the involved muscles may be due to the activity in the respective innervating neuron pools. Testing of the mesencephalon (Oculomotor) activity and the pontine (Abducens) activity may give an indication which of overactivity or underactivity may be occurring.

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References

Carrick F.R. Changes in brain function after manipulation of the cervical spine. J. Manipulative Physiol. Ther.. 1997;20:529-545.

Chusid J.G. Correlative Neuroanatomy and Functional Neurology. Los Altos, California: Lange Medical Publishers, 1964.

DeMyer W.E. Technique of the Neurologic Examination: A Programmed Text, fourth ed. New York: McGraw-Hill, 1994.

Fuller G. Neurological Examination Made Easy, third ed. New York: Churchill Livingston, 2004.

Schmid R., Wilhelm B., Wilhelm H. Naso-temporal asymmetry and contraction aniscoria in the pupillomotor system. Graefes Arch. Clin. Exp. Ophthalmol.. 2000;238(2):123-128.

Sexton, S.G., 2006. Forehead temperature asymmetry: A potential correlate of hemisphericity (Personal communication).

Further reading

Bickley L., Hoekelman R. Bates’ Guide to Physical Examination and History Taking, seventh ed. Philadelphia: Lippincott Wilkins and Williams, 1999.

Blumenfeld H. Neuroanatomy from clinical cases. Sunderland, MA: Sinauer Associates, 2002.

DeMyer W.E. Technique of the Neurologic Examination: A Programmed Text, fourth ed. New York: McGraw-Hill, 1994.

Fuller G. Neurological Examination Made Easy, third ed. New York: Churchill Livingston, 2004.

Patten J. Neurological Differential Diagnosis, second ed. New York: Springer, 2004.

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