Veda V. Vedanarayanan, MD, FRCPC
CHAPTER CONTENTS
◦Disorders with Specific Sensory Disturbances
•Localization of Motor and Sensory Disturbance
•Clinical Scenarios in Hospital Neurology
•Approach to Diagnosis of Motor and Sensory Disturbance
◦Evaluation in the Emergency Department
◦Evaluation in the Intensive Care Units
◦Anesthetic Complications from Neuromuscular Disorders
◦Patients with Tumors and Organ Transplantation
◦Patients with Rheumatologic disorders
OVERVIEW
This section discusses approach to localization and diagnoses, and this chapter focuses on motor and sensory disturbances.
MOTOR DISTURBANCE
The differential diagnosis for weakness can by quite broad. Narrowing the differential diagnosis starts with a complete history and determining the onset, distribution, and course of the weakness. The examination then determines the type of motor disorder.
Types
Motor disorders can be broadly divided into the following categories:
Weakness has the broadest potential localization. Corticospinal tract involvement is most common. Other localizations include basal ganglia, motor nerve, neuromuscular junction, and muscle.
Incoordination also has a broad potential localization. Corticospinal tract, basal ganglia, and cerebellar lesions are most common, although incoordination can occasionally be manifest by other lesions: for example, neuropathy can produce poorly coordinated movements especially if fairly acute or subacute (e.g., acute inflammatory demyelinating polyneuropathy [AIDP]).
Stiffness can be pyramidal or extrapyramidal. Corticospinal tract dysfunction produces flaccidity acutely but ultimately spasticity. Extrapyramidal conditions such as parkinsonism produces stiffness that is clinically distinct from corticospinal dysfunction.
Abnormal movements run the gamut from tremor to seizure. Determining the type of abnormal movement further localizes the lesion.
Physiologic Localization
Corticospinal lesions produce flaccid weakness initially but ultimately produce spasticity. Reflexes are eventually enhanced, although they will not be acutely. Plantar responses are often extensor immediately on clinical presentation in the ED.
Extrapyramidal lesions can produce increased tone with Parkinsonism and a host of related disorders.
Cerebellar lesions produce incoordination rather than weakness although tone may be reduced.
Motor nerve lesions produce weakness with features dependent on localization:
•Upper motoneuron lesions produce brisk reflexes, clonus, extensor plantar responses, bowel/bladder compromise, and spasticity.
•Lower motoneuron lesions can produce flaccid weakness, depressed or absent reflexes, and prominent muscle atrophy.
Neuromuscular junction lesions produce weakness and fatigue with no sensory symptoms. Reflexes are normal or reduced, depending on the severity of the weakness.
Muscle lesions produce weakness with reduced tone. Reflexes are normal or reduced depending on severity.
Anatomic Localization
Generalized motor disturbance has a broad differential diagnosis. In this case, differentiation between corticospinal, motor nerve, extrapyramidal, muscle, or neuromuscular junction narrows the diagnosis substantially. Few focal lesions produce generalized motor disturbance, although multifocal lesions commonly do.
Focal motor disturbance has a narrower differential diagnosis, although some disorders that produce generalized deficits can initially present with focal findings (e.g., parkinsonism or amyotrophic lateral sclerosis [ALS]).
SENSORY DISTURBANCE
Sensory disturbances can be more vague and subjective than motor disturbance.
Types
Sensory loss is sometimes referred to as numbness, although there are varying lay meanings for this term; some patients use numbness to mean abnormal sensation, pain, or even weakness.
Abnormal sensation is distortion of sensory input. Among these are paresthesias (abnormal spontaneous sensation) and dysesthesias (unpleasant sensation to a nonpainful stimulus). These are most commonly due to damage to the peripheral nerves. However, they can be due to lesions in the spinal cord or brain.
Neuropathic pain is produced by abnormal discharge in nociceptive and non-nociceptive afferents that is interpreted as painful. These manifestations can include hyperesthesia (enhanced sensory experience that can be perceived as discomfort) and hyperpathia (enhanced pain experience). Almost any cause of peripheral nerve damage can produce neuropathic pain.
Sensory ataxia is produced by abnormal sensory input. It can resemble cerebellar ataxia but without other cerebellar signs and with marked exacerbation with eyes closed (i.e., positive Romberg).
Localization
Generalized sensory disturbance is most commonly due to lesions in the peripheral nerves. Polyneuropathy is most common.
Focal sensory disturbance can be due to a lesion at any level. Specifics of the deficits and correlation with motor and reflexes abnormalities narrows the localization (see Table 4.1).1
Table 4.1 Localization of sensory deficits
| Abnormality | Features | Lesion | Potential cause |
| Distal sensory deficit | Sensory loss with or without pain distal on the legs; arms may be affected | Peripheral nerve | Peripheral neuropathy |
| Proximal sensory deficit | Sensory loss on trunk, without limb symptoms | Neuropathy with predominantly proximal involvement | Porphyria, diabetes, plexopathies |
| Dermatomal distribution of pain and/or sensory loss | Pain and/or sensory loss in the distribution of a single nerve root | Nerve root | Radiculopathy due to disc, osteophyte, tumor, herpes zoster |
| Single-limb sensory deficit | Loss of sensation on one limb that spans neural and dermatomal distributions | Plexus or multiple single nerves | Autoimmune plexitis, hematoma, tumor |
| Hemisensory deficit | Loss of sensation on one side of body. May be associated with pain. | Thalamus, cerebral cortex, or projections. Brainstem lesion, spinal cord lesion. Lower lesions do not involve face | Infarction, hemorrhage, demyelinating disease, tumor, infection |
| Crossed sensory deficit: ipsilateral facial and contralateral body | Pain and temperature disturbance of the ipsilateral face and contralateral body. | Lesions of uncrossed trigeminal fibers and crossed spinothalamic fibers | Lateral medullary syndrome |
| Pain/temperature vs vibration/proprioception deficits on opposite sides | Unilateral loss of pain and temperature sensation and contralateral loss of vibration and proprioception sensation. | Spinal cord lesion ipsilateral to vibration and proprioception deficit and contralateral to pain and temperature deficit | Disc protrusion, spinal stenosis, intra-spinal tumor, transverse myelitis; intraparenchymal lesions are more likely to produce dissociated sensory loss. |
| Dissociated suspended sensory deficit | Loss of pain and temperature sensation on one or both sides, with normal sensation above and below | Intramedullary lesion of cervical or thoracic spinal cord | Syrinx, chiari malformation, hydromyelia, central spinal cord tumor, or hemorrhage |
| Sacral sparing | Preservation of perianal sensation, with impaired sensation in legs and trunk | Lesion of the cord, with mainly central involvement sparing peripherally located sacral ascending fibers | Cord trauma, intrinsic tumors of the cord |
Modified From Misulis KE, Murray EL Table 30.4 from Chapter 30 Sensory Abnormalities of the Limbs, Trunk, and Face, from Bradley’s Neurology in Clinical Practice, Daroff RB, Jankovic J, Maziotta JC, Pomeroy SL Eds. Elsevier 2015
