Hemiplegia and Monoplegia

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Chapter 23 Hemiplegia and Monoplegia

Karl E. Misulis

Anatomy and Pathophysiology

Accurate neurological diagnosis begins with anatomical localization. Many disorders have diffuse localizations, but hemiplegia and monoplegia are likely to be due to focal structural lesions and are therefore easier to localize. Imaging studies often are confirmatory of the structural lesion, but clinical localization must precede and direct the imaging studies.

Hemiplegia and monoplegia are motor symptoms and signs, but associated sensory abnormalities are an aid to localization, so these are discussed when appropriate. Sensory deficit syndromes are discussed in more depth in Chapter 28. Motor power begins with volition, the conscious effort to initiate movement. Lack of volition does not produce weakness but rather results in akinesia. Projections from the premotor regions of the frontal lobes to the motor strip result in activation of corticospinal tract (CST) neurons. The descending fibers pass through the internal capsule and the cerebral peduncles, and then remain in the ventral brainstem before crossing in the medulla at the pyramidal decussation. Most of the CST crosses at this point, although a small subset of CST axons remains uncrossed until these axons reach the spinal segmental levels. Descending CST axons project to the spinal cord segments, where the fibers exit the CST and enter the spinal gray matter. Here, motoneurons are activated that then conduct action potentials via the motor axons to the muscle to produce muscle contraction.

Localization begins with identification of weakness. Differentiation is made among the following distributions:

Only hemiplegia and monoplegia are discussed in this chapter.

Hemiplegia

Cerebral Lesions

Cerebral lesions constitute the most common cause of hemiplegia. Lesions in either cortical or subcortical structures may be responsible for the weakness (Table 23.1).

Table 23.1 Cerebral Lesions

Lesion Location	Symptoms	Signs
Motor cortex	Weakness and poor control of the affected extremity, which may involve face, arm, and leg to different degrees	Incoordination and weakness that depends on the location of the lesion within the cortical homunculus; often associated with neglect, apraxia, aphasia, or other signs of cortical dysfunction
Internal capsule	Weakness that usually affects the face, arm, and leg almost equally	Often associated with sensory impairment in same distribution
Basal ganglia	Weakness and incoordination on the contralateral side	Weakness, often without sensory loss; no neglect or aphasia
Thalamus	Sensory loss	Sensory loss with little or no weakness

Cortical Lesions

Cortical lesions produce weakness that is more focal than the weakness seen with subcortical lesions. Fig. 23.1 is a diagrammatic representation of the surface of the brain, showing how the body is mapped onto the surface of the motor sensory cortex; this is the homunculus. The face and arm are laterally represented on the hemisphere, whereas the leg is draped over the top of the hemisphere and into the interhemispheric fissure.

Fig. 23.1 Representation of the body on the motor cortex. Face and arms are represented laterally, and legs are represented medially, with cortical representation of the distal legs bordering on the central sulcus.

Small lesions of the cortex can produce prominent focal weakness of one area, such as the leg or the face and hand, but hemiplegia—paralysis of both the leg and the arm on the same side of the body—is not expected from a cortical lesion unless the damage is extensive. The most likely cause of cortical hemiplegia would be a stroke involving the entire territory of the internal carotid artery.

Infarction

Infarction usually is a clinical diagnosis but can be confirmed by CT or MRI scans, as discussed earlier (see Cortical Lesions). Infarction manifests with acute onset of deficit, although the course may be one of steady progression or stuttering. Lacunar infarctions are more likely than cortical infarctions to be associated with a stuttering course.

Lenticulostriate Arteries

Lenticulostriate arteries are small penetrating vessels that arise from the proximal MCA and supply the basal ganglia and internal capsule. Infarction commonly produces contralateral hemiparesis with little or no sensory involvement. This is one cause of the syndrome of pure motor stroke, which can also be due to a brainstem lacunar infarction (Lastilla, 2006).

Thalamoperforate Arteries

Thalamoperforate arteries are small penetrating vessels that arise from the PCAs and supply mainly the thalamus. Infarction in this distribution produces contralateral sensory disturbance but also can cause movement disorders such as choreoathetosis or hemiballismus; hemiparesis is not expected.

Demyelinating Disease

Demyelinating disease comprises a group of conditions whose pathophysiology implicates the immune system.

Multiple Sclerosis

Multiple sclerosis (MS) manifests with any combination of white-matter dysfunction. Hemiparesis can develop, especially if large plaques affecting the CST fibers in the hemispheres are present. Hemiparesis is even more likely with brainstem or spinal demyelinating lesions, because smaller lesions can produce more profound deficits in these areas. The diagnosis is suggested by the progression over days plus a prior history of episodes of relapsing and remitting neurological deficits. Episodes of weakness that last for only minutes are likely not to be due to demyelinating disease but rather to transient ischemic attack (TIA) or migraine equivalent.

Diagnosis is based on clinical grounds for most patients, but the finding of areas of increased signal intensity on MRI T2-weighted images is suggestive for MS. Active demyelinating lesions often show enhancement on gadolinium-enhanced T1-weighted images. Cerebrospinal fluid (CSF) examination usually is performed and can give normal findings or show elevated protein, a mild lymphocytic pleocytosis, or oligoclonal bands of immunoglobulin G (IgG) in the CSF.

Acute Disseminated Encephalomyelitis

Acute disseminated encephalomyelitis (ADEM) is a demyelinating illness that is monophasic but in other respects manifests like a first attack of MS (Wingerchuk, 2006). This entity sometimes is called parainfectious encephalomyelitis, although the association with infection is not always certain. Symptoms and signs at all levels of the central nervous system (CNS) are common, including hemiparesis, paraplegia, ataxia, and brainstem signs. Diagnosis is based on clinical grounds, because MRI scans cannot definitively distinguish between MS and ADEM. CSF examination may show a mononuclear pleocytosis and elevation in protein, but these findings are neither always present nor specific. Even the presence or absence of oligoclonal IgG in the CSF cannot differentiate between ADEM and MS. Patients who present clinically with ADEM should be warned of the possibility of having recurrent events indicative of MS.

Progressive Multifocal Leukoencephalopathy

Progressive multifocal leukoencephalopathy (PML) is a demyelinating disease caused by reactivation of the JC virus, usually seen in immunodeficient patients. Predisposed patients include those with acquired immunodeficiency syndrome (AIDS), leukemia, lymphoma, tuberculosis, and sarcoidosis. Visual loss is the most common presenting symptom and weakness the second. MRI scan shows multiple white-matter lesions. CSF examination either reveals no abnormality or shows a lymphocytic pleocytosis or elevated protein, or both. Brain biopsy is required for specific diagnosis, although JC virus deoxyribonucleic acid (DNA) can be detected in the CSF by polymerase chain reaction (PCR) assay in most patients.

Migraine

Migraine can be divided into many subdivisions, including the following:

All but common migraine can cause hemiplegia (Black, 2006). Common migraine is episodic headache without aura; by definition, there should be no deficit. Classic migraine is episodic headache with aura, most commonly visual. Basilar migraine is episodic headache with brainstem signs including vertigo and ataxia; this variant is a disorder mainly of childhood. Complicated migraine is that in which the aura lasts for hours or days beyond the duration of the headache. Hemiplegic migraine, as its name suggests, is characterized by paralysis of one side of the body, typically with onset before the headache; this variant often is familial. Migraine equivalent is characterized by the presence of episodic neurological symptoms without headache.

Migrainous infarction features sustained deficit plus MRI evidence of infarction that had developed from the migraine. Definitive diagnosis is problematic because patients with migraine have a higher incidence of stroke not associated with a migraine attack, so the onset of the deficit with this variant should resemble classic or complicated migraine, rather than the acute deficit of most strokes.

The diagnosis of migraine is suggested by the combination of young age of the patient with few risk factors, and a marching deficit that can be conceptualized as migration of spreading electrical depression across the cerebral cortex. Imaging often is necessary to rule out hemorrhage, infarction, and demyelinating disease.

Seizures

Postictal contralateral hemiplegia or hemiparesis can occur in patients with a unilateral hemispheric seizure disorder. This situation is identified by history and slowing on the electroencephalogram (EEG) contralateral to the side of weakness.

Tumors

Tumors affecting the cerebral hemispheres commonly present with progressive deficits including hemiparesis. Coordination deficit commonly develops before the weakness. Cortical dysfunction is commonly present, such as aphasia with dominant hemisphere lesions and neglect. Other signs of expanding tumors may include headache, seizures, confusion, and visual field defects.

Tumor should be suspected in a patient with progressive motor deficit over weeks, especially with coexistent seizures or headache. MRI with contrast enhancement is more sensitive than CT for identification of tumors.

Alternating Hemiplegia of Childhood

Alternating hemiplegia of childhood is a rare condition characterized by attacks of unilateral weakness, often with signs of other motor deficits (e.g., dyskinesias, stiffness) and oculomotor abnormalities (e.g., nystagmus) (Zhang et al., 2003). Attacks begin in young childhood, usually before age 18 months; they last hours, and deficits accumulate over years. Initially, patients are normal, but with time, neurological deficits including motor deficits and cognitive decline become obvious. A benign form can occur on awakening in patients who are otherwise normal and do not develop progressive deficits; this entity is related to migraine. Diagnostic studies often are performed, including MRI, electroencephalography, and angiography, but these usually show no abnormalities. Alternating hemiplegia is suggested when a young child presents with episodes of hemiparesis, especially on awakening, not associated with headache.

Hemiconvulsion-Hemiplegia-Epilepsy Syndrome

In young children with the rare condition called hemiconvulsion-hemiplegia-epilepsy syndrome, unilateral weakness develops after the sudden onset of focal seizures. The seizures are often incompletely controlled. Neurological deficits are not confined to the motor system and may include cognitive, language, and visual deficits. Unlike alternating hemiplegia, the seizures and motor deficits are consistently unilateral, although eventually the unilateral seizures may become generalized. Imaging findings may be normal initially, but eventually atrophy of the affected hemisphere is seen (Freeman et al., 2002). CSF analysis is not specific, but a mild mononuclear pleocytosis may develop because of the CNS damage and seizures. Rasmussen encephalitis is a cause of this syndrome.

Brainstem Lesions

Brainstem lesions producing hemiplegia are among the easiest to localize because associated signs of cranial nerve and brainstem dysfunction are almost always present.

Brainstem Motor Organization

Fig. 23.2 shows the anatomical organization of the motor systems of the brainstem. Discussion of the complex anatomical organization of the brainstem can be simplified by concentrating on some important functions:

Appendicular motor and sensory function

Appendicular coordination

Facial motor and sensory function

Ocular motor function

Descending sympathetic tracts

Fig. 23.2 Brainstem motor organization, beginning with internal capsule. Corticospinal tract remains topographically organized throughout brainstem and spinal cord, although isolated lesions below cerebral cortex are unlikely to produce topographically specific damage.

Motor pathways descend through the CST to the pyramidal decussation in the medulla, where they cross to innervate the contralateral body. Lesions of the pons and midbrain above this level produce contralateral hemiparesis, which may involve the contralateral face. Rostral lesions of the medulla produce contralateral weakness, whereas more caudal medullary lesions produce ipsilateral cranial nerve signs with a contralateral hemiparesis and sensory deficit.

Sensory pathways from the nucleus gracilis and nucleus cuneatus cross at about the same level as the motor fibers of the CST, so deficits in light touch and position sense tend to parallel the distribution of the motor deficit. By contrast, the spinothalamic tracts have already crossed in the spinal cord and ascend laterally in the brainstem. Accordingly, lesions of the lower medulla may produce contralateral loss of pain and temperature sensation and ipsilateral loss of touch and position sense. Lesions above the mid-medulla produce a contralateral sensory defect of all modalities similar to that from cerebral lesions, yet the clues to brainstem localization can include the following:

Ipsilateral facial sensory deficit from a trigeminal lesion

Ipsilateral hemiataxia from damage to the cerebellar hemispheres or nuclei

Ocular motor weakness from any of multiple lesion locations

Ipsilateral Horner syndrome from damage of the descending sympathetic tracts

Common Lesions

Table 23.2 shows some of the important lesions of the brainstem and their associated motor deficits. Brainstem lesions usually are due to damage to the penetrating branches of the basilar artery. Patients present with contralateral weakness along with other deficits that help localize the lesion. Hemiataxia often develops and can be mistaken for hemiparesis, so careful examination is essential. Demyelinating disease and tumors are the other most common causes of brainstem dysfunction.

Table 23.2 Brainstem Lesions

Named Disorder	Lesion Location	Signs
MIDBRAIN
Weber syndrome	CN III, ventral midbrain, CST	Contralateral hemiparesis, CN III palsy
Benedikt syndrome	CN III, ventral midbrain, CST, red nucleus	Contralateral hemiparesis, third nerve palsy, intention tremor, cerebellar ataxia
Top-of-the-basilar syndrome	Occipital lobes, midbrain oculomotor nuclei, cerebral peduncle, medial and temporal lobe, thalamus	Contralateral hemiparesis, cortical blindness, oculomotor deficits, memory difficulty, contralateral sensory deficit
PONS
Millard-Gubler syndrome	CN VI, CN VII, ventral pons	Contralateral hemiparesis, CN VI and CN VII palsies
Clumsy hand syndrome	CST, CN VII	Contralateral hemiparesis, dysarthria, often with facial weakness
Pure motor hemiparesis (due to pons lesion)	Ventral pons	Contralateral hemiparesis with corticospinal tract signs
Ataxic hemiparesis (due to pons lesion)	CST, cerebellar tracts	Contralateral hemiparesis with impaired coordination
Foville syndrome	CN VII, ventral pons, paramedian pontine reticular formation	Ipsilateral CN VII palsy, contralateral hemiparesis, gaze palsy to the side of the lesion
MEDULLA
Medial medullary syndrome	CST, medial lemniscus, hypoglossal nerve	Contralateral hemiparesis, loss of position and vibratory sensation, ipsilateral tongue paresis
Lateral medullary syndrome	Spinothalamic tract, trigeminal nucleus, cerebellum and inferior cerebellar peduncle, vestibular nuclei, nucleus ambiguus	No hemiparesis usually produced, but hemiataxia may be mistaken for hemiparesis; dysphagia, hemisensory loss, face weakness, Horner syndrome are common

CN, Cranial nerve; CST, corticospinal tract.

Spinal Lesions

Spinal lesions can produce hemiplegia sparing the face, although they mostly will cause bilateral deficits typical of myelopathy. A spinal cord lesion should be suspected in a patient with bilateral weakness, bowel or bladder control deficits, and back pain.

Spinal Hemisection (Brown-Séquard Syndrome)

Spinal hemisection seldom is seen in clinical practice. Components of the syndrome occasionally are identified, however. This entity is usually associated with intradural tumors, trauma, inflammatory conditions such as demyelinating disease, and occasionally spinal infarction. Spondylotic myelopathy, disk disease, and most extradural tumors typically produce symmetrical deficits. Patients with the spinal hemisection syndrome present with weakness ipsilateral to and below the lesion. In addition, segmental motor loss may be seen with involvement of the motoneurons at the level of the lesion. Sensory abnormalities include loss of pain and temperature contralateral to and below the lesion. Position sense may be affected ipsilateral to the lesion.

Transverse Myelitis

Transverse myelitis is an acute myelopathic process that is presumed to be autoimmune in origin. Patients present with motor and sensory deficits below the lesion, usually in the form of a paraplegia. The abnormalities typically are bilateral but may be asymmetrical. MRI may show enhancement in the spinal cord, which has an appearance that differs subtly from that in involvement in MS. CSF analysis is nondiagnostic.

Transverse myelitis is a clinical diagnosis. The primary differential diagnosis is between MS and neuromyelitis optica (NMO); assessment to identify the latter includes measurement of titers of NMO antibodies in the plasma, which probably should be done in all patients with transverse myelitis.

Spinal Cord Compression

Spinal cord compression usually is due to disk protrusion, spondylosis, or acute trauma, but neoplastic and infectious causes should always be considered (Shedid and Bonzel, 2007). Disc disease and spondylosis typically are in the midline, so bilateral findings are expected. Extradural tumors also usually produce bilateral findings. Intradural tumors may produce unilateral deficits and occasionally can manifest as Brown-Séquard syndrome.

Lesions below the cervical spinal cord would produce not hemiplegia but rather monoplegia of a lower limb or paraplegia. Spondylosis with cord compression produces lower motor neuron (LMN) weakness at the level of the lesion and CST signs below the level of the lesion. Spinal cord compression resulting in paralysis should be evaluated as quickly as possible with MRI. Myelography should be considered if MRI is not urgently available.

Spinal Cord Infarction

Anterior spinal artery infarction usually causes paraparesis and spinothalamic sensory loss below the level of the lesion; dorsal column function is preserved. Rarely, one segmental branch of the anterior spinal artery can be involved with unilateral spinal cord damage and monoparesis or hemiparesis. Spinal cord infarction is suggested when a patient presents with paraparesis or paraplegia of acute onset, and MRI does not show cord compression or bilateral ACA infarction.

Peripheral Lesions

Peripheral lesions are not expected to produce hemiplegia. A pair of peripheral lesions affecting an arm and leg on the same side, however, may occasionally masquerade as hemiplegia. Differentiation depends on identification of the individual lesions as being within the distribution of one nerve, nerve root, or plexus division. The tendon reflexes are likely to be depressed in patients with peripheral lesions, rather than increased as with CST lesions.

Amyotrophic lateral sclerosis can produce weakness of one limb, followed by weakness of the other limb on the same side, with progression over months or even years. Usually the combined presence of upper motor neuron (UMN) and LMN involvement without sensory changes assists in making the diagnosis. If the predominant involvement is UMN in type, the picture can look like that of a progressive hemiparesis.

Mononeuropathy multiplex can manifest as separate lesions affecting individual limbs; involvement of an arm and leg on the same side can give the impression of hemiparesis. Diabetes is the most common cause, but other causes include leprosy, vasculitis, and predisposition to pressure palsies. Diagnosis is by electromyography (EMG), which can differentiate mononeuropathies from polyneuropathy (Misulis, 2003). Radiculopathy would not give hemiparesis but is a consideration in the differential diagnosis for monoplegia (see Radiculopathies, later in this chapter).

Functional Hemiplegia

Functional or psychogenic weakness includes both conversion reaction and malingering. In conversion reaction, the patient is not conscious of the nonorganic nature of the deficit, whereas in malingering, the patient is making a conscious effort to fool the examiner. Some secondary gain for the patient, either psychological or economic, is a factor with both types. In malingering, the secondary gain usually is more obvious and may be disability payments, litigation, family attention, or avoidance of stressors or tasks. Clues to functional weakness include the following:

Improvement in strength with coaching

Give-way weakness

Inconsistencies in examination—for example, inability to extend the foot but able to walk on toes

Hoover sign (when the patient lies supine on the bed and lifts one leg at a time, the examiner should feel effort to press down with the opposite heel if the leg is truly paralyzed; failure to do so constitutes the Hoover sign)

Paralysis in the absence of other signs of motor system dysfunction, including tone and reflex changes

Diagnosis of functional weakness is based on inconsistencies on examination and elimination of the possibility of organic disease. Functional weakness should be diagnosed with caution. It is easy to dismiss the patient’s complaints after an inconsistent feature is seen, especially if some secondary gain is obvious. Unfortunately, a patient with organic problems may have a functional overlay, which may exaggerate otherwise subtle clinical findings.

If functional weakness is suspected, some diagnostic testing often is required to rule out neurological disease, although such investigations should be kept to a minimum. Prescription of multiple tests and treatments may serve to reinforce the presumed presence of disease, thereby augmenting illness behavior. Psychological evaluation and treatment can be key to successful management. Nevertheless, functional deficit probably is overdiagnosed, so the examiner should remain alert for organic disease.

Monoplegia

Cerebral Lesions

Cerebral lesions more commonly produce hemiplegia than monoplegia, but isolated limb involvement can occasionally occur, especially with cortical involvement. The arm segment of the motor-sensory cortex lies on the lateral aspect of the hemisphere adjacent to the sylvian fissure. Subcortical lesions are less likely than cortical lesions to produce monoplegia because of the dense packing of the fibers of the CST in the internal capsule. The internal capsule generally is organized with the arm segments represented anteriorly in the capsule relative to the leg sections. Infarction in the distribution of the lenticulostriate arteries, however, usually affects both divisions.

Infarction

The arm region of the motor cortex is supplied by the MCA. Infarction of a branch of the MCA can produce isolated arm weakness, although facial involvement and cortical signs are expected—language deficit with left hemisphere lesions and neglect with right hemisphere lesions (Paciaroni et al., 2005). With more extensive lesions, visual fields can be abnormal because of infarction of the optic radiations. Mild leg weakness also can occur with medial cortical involvement of the infarct. The leg segment of the cortex lies in the parasagittal region and is supplied by the ACA. ACA infarction produces weakness of the contralateral leg.

Transient Ischemic Attack

Episodic paralysis of one limb sometimes is due to TIA. Evaluation for vascular disease usually is indicated. The main considerations in the differential diagnosis are migraine and seizure. Abrupt onset and absence of positive motor symptoms argue in favor of TIA.

Migraine

Migraine can produce sensation that marches along one limb, usually the arm. This marching pattern differs from the abrupt onset of stroke. Involvement of only the leg is unusual. The headache phase typically begins as the neurological deficit is resolving. Weakness can develop as part of the migraine aura, but this is much less likely than sensory disturbance. Of note, not all migrainous weakness is followed by headache.

Seizure

Seizure classically produces positive motor symptoms with jerking or stiffness. Focal seizures rarely can produce negative motor symptoms including paralysis. In such cases, the seizure can be impossible to diagnose without EEG, so EEG may be indicated in selected patients with focal weakness. Ictal paralysis can have abrupt onset and offset and can even resemble negative myoclonus.

Focal seizure activity may be suggested by subtle twitching or disturbance of consciousness associated with the episodes. In comparison with TIAs, seizures usually are more frequent and have a shorter duration. Lastly, postictal weakness of one limb can occur.

Multiple Sclerosis

Multiple Sclerosis can produce monoplegia secondary to a discrete white-matter plaque in the cerebral hemisphere, but because it is a subcortical disease, hemiparesis is more common. The corticospinal tracts are somatotopically organized, so monoparesis is theoretically possible. Onset of symptoms is subacute. MS is considered when a patient with neurological deficit is found to have multifocal lesions on clinical examination or MRI.

Tumors

Tumors deep to the cortex rarely produce monoplegia because the involvement is not sufficiently discrete to affect only one limb. Cortical involvement makes single-limb involvement more likely. Parasagittal lesions often produce leg involvement, which initially can be unilateral. Meningiomas often arise from one side of the falx, so they predominantly affect the opposite leg, initially with weakness, incoordination, and CST signs. With progression, bilateral symptoms develop.

Bilateral leg weakness with CST signs can be due to either cerebral or spinal lesions, although single leg deficit is only rarely due to a spinal cause. Metastatic tumors often are found at the gray/white junction; in this location, they can produce focal cortical damage. Early on, the lesion may be too small to produce other neurological symptoms, but with increasing growth, it is more likely to produce focal seizures. Tumor is suspected with insidious progression of focal deficit, especially if combined with headache or seizures.

Brainstem Lesions

Brainstem lesions seldom produce monoplegia because of the tight packing of the fibers of the CSTs in the brainstem. Unilateral cerebellar hemisphere lesions may produce appendicular ataxia, which is most obvious in the arm, although this should be distinguished from monoparesis by the absence of weakness or CST signs.

Spinal Lesions

Spinal lesions can produce weakness from segmental damage to nerve roots or CSTs. Weakness at the level of the lesion is in a radicular distribution and may be associated with muscle atrophy and loss of segmental reflexes. Weakness below the lesion can be unilateral or bilateral and is associated with CST signs.

Peripheral Lesions

Peripheral lesions usually produce monoparetic weakness in the distribution of a single nerve, nerve root, or plexus. A few conditions, such as amyotrophic lateral sclerosis and focal spinal muscular atrophy, may produce weakness in a monomelic (monoplegic) distribution.

Pressure Palsies

Intermittent compression of a peripheral nerve can produce transient paresis of part of a limb. The patient may think the entire limb is paralyzed, but detailed examination shows that the paresis is limited to a nerve distribution. Recovery from the weakness usually occurs so rapidly that examination often is not possible before the improvement. Predisposition to pressure palsies can be seen in two main circumstances: on a hereditary basis and in the presence of peripheral polyneuropathy.

Hereditary Neuropathy with Predisposition to Pressure Palsies

Hereditary neuropathy with predisposition to pressure palsies is associated with episodic weakness and sensory loss associated with compression of isolated nerves. This disorder is inherited as an autosomal dominant condition. Nerve conduction studies may show distal slowing of conduction velocities in affected nerves. NCVs also may be reduced in asymptomatic gene carriers (Chance, 2006).

Pressure Palsies in Polyneuropathy

Patients with polyneuropathy may have an increased susceptibility to pressure palsies. Areas of demyelination are more likely to have a depolarizing block produced by even mild pressure.

Mononeuropathies

Table 23.3 shows some important peripheral nerve lesions of the arm. Table 23.4 shows some important peripheral nerve lesions of the leg.

Table 23.3 Peripheral Nerve Lesions of the Arm

Lesion	Clinical Findings	Electromyography Findings
MEDIAN NEUROPATHY
Carpal tunnel syndrome	Weakness and wasting of abductor pollicis brevis if severe; sensory loss on palmar aspect of first through third digits	Slow median motor and sensory NCV through the carpal tunnel; denervation of abductor pollicis brevis if severe
Anterior interosseous syndrome	Weakness of flexor digitorum profundus, pronator quadratus, flexor pollicis longus	Denervation in flexor digitorum profundus, flexor pollicis longus, pronator quadratus
Pronator teres syndrome	Weakness of distal median-innervated muscles; tenderness of pronator teres	Slow median motor NCV through proximal forearm denervation of distal median-innervated muscles
Compression at the ligament of Struthers	Weakness of distal median-innervated muscles	As for pronator teres syndrome, with the addition of denervation of pronator teres
ULNAR NEUROPATHY
Palmar branch damage	Weakness of dorsal interossei; no sensory loss	Normal ulnar NCV; denervation of first dorsal interosseus but not abductor digiti minimi
Entrapment at Guyon canal	Weakness of ulnar intrinsic muscles; numbness over fourth and fifth digits	Slow ulnar motor and sensory NCV through wrist
Entrapment at or near the elbow	Weakness of ulnar intrinsic muscles; numbness over fourth and fifth digits	Slow ulnar motor NCV across elbow, denervation in first dorsal interosseus, abductor digiti minimi, and ulnar half of flexor digitorum profundus
RADIAL NEUROPATHY
Posterior interosseus syndrome	Weakness of finger and wrist extensors; no sensory loss	Denervation in wrist and finger extensors; sparing of the supinator and extensor carpi radialis
Compression at the spiral groove	Weakness of finger and wrist extensors; triceps usually spared; sensory loss on dorsal aspects of first digit	Slow radial motor NCV across spiral groove; denervation in distal radial-innervated muscles; triceps may be affected with proximal lesions

NCV, Nerve conduction velocity.

Table 23.4 Peripheral Nerve Lesions of the Leg

Lesion	Clinical Findings	Electromyography Findings
Sciatic neuropathy	Weakness of tibial- and peroneal-innervated muscles, with sensory loss on posterior leg and foot	Denervation distally in tibial- and peroneal-innervated muscles
Peroneal neuropathy	Weakness of foot extension and eversion and toe extension	Denervation in tibialis anterior; NCV across fibular neck may be slowed
Tibial neuropathy	Weakness of foot plantar flexion	Denervation of gastrocnemius
Femoral neuropathy	Weakness of knee extension; weakness of hip flexion if psoas involved	Denervation in quadriceps, sometimes psoas

NCV, Nerve conduction velocity.

Median Nerve

The most common median neuropathy is carpal tunnel syndrome, but other important anatomical lesions including anterior interosseus syndrome and pronator teres syndrome have been described.

Carpal Tunnel Syndrome

Carpal tunnel syndrome is the most common mononeuropathy. The median nerve is compressed as it passes under the flexor retinaculum at the wrist. Patients present with numbness on the palmar aspect of the first through the third digits. Forced flexion or extension of the wrist commonly exacerbates the sensory symptoms. Weakness of the abductor pollicis brevis may develop in advanced cases.

This condition would not normally be considered in the differential diagnosis for monoparesis, but because the patient can complain of weakness that is more extensive than the actual deficit, it is considered here. Nerve conduction studies show slow motor and sensory velocities through the carpal tunnel. EMG shows denervation in the abductor pollicis brevis muscle with severe disease.

Anterior Interosseus Syndrome

The anterior interosseous nerve is a branch of the median nerve in the forearm that supplies some of the forearm muscles. Damage can occur distal to the elbow, producing a syndrome that essentially is purely motor. Weakness of finger flexion is prominent. Affected muscles include the flexor digitorum profundus to the second and third digits (the portion to the fourth and fifth digits is innervated by the ulnar nerve). The distal median nerve entering the hand is unaffected because the anterior interosseous nerve arises from the main trunk of the median nerve.

Diagnosis is suspected by weakness of the median nerve–innervated finger flexors, with sparing of the abductor pollicis brevis and ulnar nerve–innervated flexors. EMG can confirm the diagnosis, but because this entrapment is not commonly looked for by many electromyographers, study of the appropriate muscles must be specifically requested.

Pronator Teres Syndrome

The median nerve distal to the elbow can be damaged as it passes through the pronator teres muscle. All median-innervated muscles of the arm are affected except for the pronator teres itself. The clinical picture is that of an anterior interosseous syndrome plus distal median neuropathy. The pronator teres may be tender, and palpation may exacerbate some of the distal pain.

Ulnar Nerve

Ulnar entrapment is most common near the elbow and at the wrist. Entrapment at the elbow produces weakness of the ulnar-innervated intrinsic muscles. Weakness of long flexors of the fourth and fifth digits also can develop. When the entrapment is at the wrist, the weakness is isolated to the intrinsic muscles of the hand, and more proximal muscles are unaffected. Although most of the intrinsic muscles of the hand are ulnar innervated, a few are median innervated and are unaffected in ulnar neuropathy.

The diagnosis of ulnar neuropathy is suggested when a patient complains of pain or numbness on the ulnar aspect of the hand. Additional findings that support this diagnosis include weakness and wasting of the intrinsic muscles of the hand, which is especially easy to see in the first dorsal interosseous.

Radial Nerve Palsy

Radial neuropathy is most commonly seen above the elbow, such that wrist and finger extensors are mainly affected. The triceps also can be affected. Radial nerve palsy is most commonly due to a pressure palsy in alcoholic intoxication. Peripheral neuropathy makes the development of pressure neuropathy of the radial nerve more likely.

Femoral Neuropathy

Femoral neuropathy can occur at the origin of the nerve from the lumbar plexus secondary to compression by intraabdominal contents (fetus or neoplasm), but we also have seen it from damage incurred during angiography or surgery. Patients present with pain in the thigh and weakness of knee extension. They usually report that the leg “gives out” during walking or that they cannot get out of a chair without using their arms. Examination may show quadriceps weakness, but this muscle group is so strong that the examiner may not be able to detect the deficit. Lower leg muscles must be examined to ensure that muscles in the sciatic distribution are normal. Diagnosis is confirmed by EMG showing denervation confined to the femoral nerve distribution. Unfortunately, electrical signs of denervation may not be obvious for up to 4 weeks after the injury.

Sciatic Neuropathy

Sciatic neuropathy can have multiple causes, including acute trauma and chronic compressive lesions. The term sciatica describes pain in the distribution of the sciatic nerve in the back of the leg. It usually is due to radiculopathy (see Radiculopathies, later). An intramuscular injection into the sciatic nerve rather than the gluteus muscle is an occasional cause of sciatic neuropathy, which is characterized by initial severe pain followed by a lesser degree of pain and weakness.

Piriformis syndrome is a condition in which the sciatic nerve is compressed by the piriformis muscle. This is a difficult diagnosis to make, requiring demonstration of increased pain on tensing the piriformis muscle by flexing and adducting the hip. Piriformis syndrome should be considered in patients presenting with symptoms and signs referable to the sciatic nerve but with no evident cause seen on imaging of the lumbar spine and plexus.

Diagnosis of sciatic neuropathy is considered when a patient presents with pain or weakness of the lower leg muscles. EMG can confirm the distribution of denervation. Nerve conduction studies usually are normal. MRI of the lumbosacral plexus occasionally is needed to look for tumors and other causes of sciatic nerve or plexus compression.

Peroneal Neuropathy

Peroneal neuropathy can develop from a lesion at the fibular neck, the popliteal fossa, or even the sciatic nerve in the thigh. The peroneal division of the sciatic nerve is more susceptible to injury than the tibial division, so incomplete sciatic injury affects predominantly the peroneal nerve–innervated muscles. The peroneal nerve innervates the tibialis anterior, extensor digitorum brevis, and peroneus muscles. In addition, the peroneal division innervates the short head of the biceps femoris in the distal posterior thigh. This is an important muscle to remember because distal peroneal neuropathy spares this muscle, whereas a proximal sciatic neuropathy, a peroneal division lesion, or a radiculopathy is expected to cause denervation not only in the tibialis anterior but also the short head of the biceps femoris (Marciniak et al., 2005).

Radiculopathies

Radiculopathy produces weakness of one portion of a limb. Common radiculopathies are summarized in Table 23.5. Complete paralysis of all of the muscles of an arm or leg is not caused by radiculopathy, other than in traumatic avulsion of the nerve roots, which may occur in the upper limbs with distraction injuries of the arm from the neck. Roots serving arm power include chiefly C5 to T1. Roots serving leg power are chiefly L2 to S1. A lesion at the L5 level often elicits a complaint of weakness of the entire limb because of the foot drop, which interferes with gait. Reflex abnormalities often are present early in a radiculopathy and are a manifestation of the sensory component. Motor deficits develop with increasingly severe radiculopathy.

Table 23.5 Radiculopathies

Level	Motor Deficit	Sensory Deficit
CERVICAL RADICULOPATHY
C5	Deltoid, biceps	Lateral upper arm
C6	Biceps, brachioradialis	Radial forearm and first and second digits
C7	Wrist extensors, triceps	Third and fourth digits
C8	Intrinsic hand muscles	Fifth digit and ulnar forearm
T1	Intrinsic muscles of the hand, especially APB	Axilla
LUMBAR RADICULOPATHY
L2	Psoas, quadriceps	Lateral and anterior thigh
L3	Psoas, quadriceps	Lower medial thigh
L4	Tibialis anterior, quadriceps	Medial lower leg
L5	Peroneus longus, gluteus medius, tibialis anterior, extensor hallucis longus	Lateral lower leg
S1	Gastrocnemius, gluteus maximus	Lateral foot and fourth and fifth digits

APB, Abductor pollicis brevis.

Diagnosis of radiculopathy can be facilitated by EMG, which is an aid to localization and helps determine whether acute changes are developing. MRI shows the structural cause of a definite radiculopathy in most patients, although the diagnostic yield in patients with back pain without clear radicular symptoms is far less (see Chapters 29 and 30). Many surgeons still consider myelography followed by CT scanning to be more sensitive than MRI for detecting structural defects, although it is not performed as a first-line investigation because of the invasive nature of the procedure.

Radiculopathy should be suspected when a patient presents with pain radiating down one arm or leg, especially if neck or low back pain corresponding to the level of the deficit is a feature as well. Motor and sensory symptoms and signs should conform to one nerve root distribution.

Plexopathies

Brachial and Lumbar Plexitis (or Plexopathy)

Brachial plexitis is an acute neuropathic syndrome of presumed autoimmune etiology. Patients present with shoulder and arm pain followed by weakness as the pain abates. Eventual functional recovery is the rule, although this takes months and occasionally is incomplete. Brachial plexitis is somewhat more common than lumbosacral plexitis. The upper plexus, C5 and C6, most commonly is affected, although the lower plexus can be involved. Lumbosacral plexitis has a clinical course similar to that with brachial plexitis.

A diagnosis of plexitis is considered when a patient presents with single limb pain and weakness that does not follow a single root or nerve distribution. MRI appearance of the region is normal unless neoplastic infiltration has occurred. Findings on nerve conduction studies may be normal distally in the limbs, but F-waves will be slowed or absent. EMG findings may be normal initially, but eventually this study shows denervation in the distribution of the affected portion of the plexus.

Differentiation of plexitis from radiculopathy is accomplished on the basis of not only the more extensive deficits in patients with plexitis but also the time course of pain followed by weakness as the pain abates; this pattern is not expected in patients with radiculopathy. EMG of paraspinal muscles at the level of involvement will show denervation changes in a radiculopathy but not in a plexopathy. Sensory nerve action potentials may be lost distally in a plexopathy, but not in a radiculopathy, because of its preganglionic location, leaving the distal branches of the sensory neurons intact.

Neoplastic Plexus Infiltration

The brachial and lumbar plexuses are in proximity to the areas that can be infiltrated by tumors, including those involving the lymph nodes, lungs, kidneys, and other abdominal organs. The first symptom of tumor infiltration usually is pain. Weakness and sensory loss are less common symptoms. Neoplastic plexus compression or infiltration manifests as a progressive painful monoparesis. Limb movements that stretch the plexus elicit pain, and the patient tends to hold the limb immobile to avoid exacerbating the pain.

Neoplastic infiltration of the brachial plexus usually involves the lower plexus, C8 to T1. Lung cancer and lymphoma are the most common tumors to cause this. Horner syndrome can develop with lower brachial plexus involvement. The main consideration in the differential diagnosis is radiation plexopathy. The diagnosis is suspected on the basis of the severe pain and weakness. EMG often shows denervation that spans single nerve and root distributions. Detailed knowledge of the plexus anatomy is essential during examination and EMG. MRI usually shows the infiltration or compression of the plexus.

Radiation Plexopathy

Radiation therapy in the region of the plexus can produce progressive dysfunction. The upper brachial plexus is especially susceptible because of the lesser amount of surrounding tissues to attenuate the radiation. Symptoms are dysesthesias and weakness. The dysesthesias may be associated with discomfort but seldom are described as painful. This absence of pain is one key to differentiation from neoplastic plexus infiltration, which typically is quite painful.

Diagnosis is suspected in the clinical setting of progressive painless weakness in a patient with cancer who has received radiation to the region. MRI is essential to rule out tumor infiltration. EMG shows denervation, which is not a differentiating feature, but myokymia is more commonly seen in patients with radiation plexopathy than in those with neoplastic infiltration.

Plexopathy from Hematomas

Hematomas can develop adjacent to and compress the brachial and lumbosacral plexuses, producing motor and sensory findings. Brachial plexus hematomas are usually from bleeding disorders or instrumentation such as central line placement. Lumbosacral plexus hematomas also can develop from coagulopathies, including that associated with anticoagulant treatment, and after procedures such as abdominal surgery or femoral arterial catheterization. In the latter circumstance, blood leaking from the puncture site can flow proximally, and a substantial amount of blood may be lost without a clinically obvious hematoma.

Hematomas interfere with the function of the peripheral nerves and plexus by blocking conduction. The prognosis generally is good so long as the plexus or nerve has not been directly injured, because the condition usually is neurapraxia rather than neurotmesis, and conduction usually is restored when the blood is resorbed. Large hematomas should be evacuated if severe plexus damage is present.

Plexus Trauma

A history of trauma makes the etiology of the plexopathy quite obvious. The main difficulty is in differentiating traumatic plexopathy from radiculopathy (nerve root avulsion) or peripheral nerve damage. Also, spinal cord damage must be considered because cord contusion and hematomyelia may manifest with weakness that is more prominent in one extremity. Motor vehicle accidents, childbirth, and occupational injuries are the most common causes of traumatic plexopathy. In many cases of plexus stretch, the mechanism is forced extension of the arm over the head or forced downward movement of the shoulder. Forced extension of the arm over the head damages the lower plexus, with the intrinsic muscles of the hand being especially affected (Klumpke palsy). Forced depression of the shoulder produces damage to the upper plexus, giving prominent weakness of the deltoid, biceps, and other proximal muscles (Erb palsy).

Trauma includes not only stretch injury but also penetrating injury such as knife and bullet wounds. Knife wounds can easily damage the brachial plexus but are much less likely to involve the lumbosacral plexus. Gunshot wounds may directly affect either the brachial or lumbosacral plexus, and the shock waves of high-velocity bullets may damage the plexus without direct contact. Unfortunately, the speed and extent of recovery from these types of injuries are poor.

Diagnostic studies should include imaging not only of the plexus but also of the adjacent spinal cord, looking for disk herniation, spondylosis, subluxation, or other anatomical deformity. Plain radiographs should be obtained to ensure skeletal integrity. MRI or CT of the region will visualize the soft tissues.

Thoracic Outlet Syndrome

Thoracic outlet syndrome is an overdiagnosed condition characterized by weakness of muscles innervated by the lower trunk of the brachial plexus. The motor axons in the lower trunk supply both the median- and ulnar-innervated intrinsic muscles of the hand. Finger and wrist flexors occasionally may be affected, causing marked impairments in use of the hand, which is not restricted to a single nerve distribution. This deficit must be differentiated from that due to a cortical lesion. Sensory loss is mainly in an ulnar distribution, because the sensory fibers of the median nerve ascend through the middle trunk rather than the lower trunk.

Diagnosis of thoracic outlet syndrome depends on demonstration of low-amplitude median and ulnar nerve compound motor action potentials and ulnar sensory nerve action potentials. Median sensory nerve action potentials are normal. CT or MRI of the plexus may be necessary to rule out infiltration by nearby tumor. Imaging of the neck and cervical spine occasionally reveals cervical ribs. These usually are asymptomatic, so their presence does not confirm the diagnosis of thoracic outlet syndrome.

Diabetic Amyotrophy

Diabetic amyotrophy is one of the terms given to the syndrome of damage to the proximal lumbar plexus, serving mainly the femoral nerve, seen in diabetes mellitus. Patients present with weakness and pain in a femoral nerve distribution. Although a length-dependent diabetic peripheral neuropathy may be an accompanying feature, the femoral distribution symptoms and signs overshadow the other findings. Patients eventually improve, although the recovery often is prolonged and incomplete. It is difficult to study nerve conduction of the femoral nerve, so this test is diagnostically helpful only if results are normal. EMG usually shows denervation, although up to 4 weeks may pass before electrical signs of axonal dysfunction are seen.

Neuronopathies

Neuronal degenerations usually affect multiple individual nerve distributions and usually involve more than one limb. A few focal motor neuropathies, however, can produce single limb defects.

Monomelic Amyotrophy

Monomelic amyotrophy is a condition in which motoneurons of one limb degenerate; often the distribution suggests involvement of specific motoneuron columns in the spinal cord. It affects only one limb, usually an arm. The opposite limb can be affected to a much lesser extent. Pain and sensory loss are not features of this disorder. Progressive weakness develops over months to years and may eventually plateau without further worsening. Onset usually is in young adulthood, at the age of approximately 20 years, and men are predominantly affected. Diagnosis is confirmed by clinical presentation and EMG findings of active and chronic denervation without sensory abnormalities.

Poliomyelitis

Poliomyelitis is now uncommon but still occurs in some parts of the world. A poliomyelitis-like syndrome can result from viruses other than the poliovirus itself, including West Nile virus. The illness usually manifests with acute asymmetrical weakness after an initial phase of encephalitic symptoms including headache, meningeal signs, and possibly confusion or seizures. The paralysis may involve only one limb but more commonly is generalized. After recovery, only one limb may remain weak (monoparesis).

Pitfalls in the Differential Diagnosis for Hemiplegia and Monoplegia

Diagnosis of hemiplegia and monoplegia can always be a challenge, but identifying or localizing the underlying lesion can be especially difficult with certain clinical presentations. Some important points in the differential diagnosis with such presentations are considered next.

Focal Weakness of Apparently Central Origin

Focal Weakness That Appears to Be Central: Cerebral Cortex, Internal Capsule, Brainstem, or Spinal Cord?

Lesions in cerebral cortex, internal capsule, brainstem, and spinal cord all produce weakness due to CST dysfunction, with typical clinical findings. Note that acute lesions may not be associated with hyperreflexia and upgoing plantar response—these reflex alterations take time to develop.

Cerebral cortex lesions usually produce weakness that is most prominent in one region, such as arm, face, or leg, whereas internal capsule and brainstem lesions are more likely to produce equivalent dysfunction of the arm and leg. Cortical lesions often are associated with cortical deficits of aphasia or neglect, whereas lower lesions do not do this. Brainstem lesions commonly are associated with cranial nerve deficits, especially diplopia from disturbance of ocular motor centers. Vertigo and ataxia without weakness also suggest a brainstem lesion. Spinal cord lesions usually produce bilateral deficits below the level of the lesion, with both motor and sensory involvement. Structural lesions of the spine are almost always painful, although MS and transverse myelitis usually are not.

Focal Weakness That Appears to Be Central: Migraine, TIA, or Seizure?

Examination findings can be identical with migraine, TIA, and seizure, so clinical differentiation among these three insults rests on the history. TIA is characterized by an abrupt onset, with gradual recovery over the course of 5 minutes to 1 hour; deficits outside this time window argue in favor of alternative diagnoses—a TIA lasting hours is more likely to represent a small infarction with clinical resolution but persistent perfusion defect. The deficit of migraine evolves in keeping with the migration of spreading depression across the cerebral cortex—thus, over minutes the deficit marches from hand up arm to face, for example. Weakness with migraine usually precedes headache but may accompany headache or may even not be associated with headache in some instances. Seizure is a rare cause of transient weakness. Seizure is suggested by abrupt onset and offset of the deficit, and any associated symptoms of decreased response or twitching.

Weakness of the Hand and Wrist

Weakness in Intrinsic Muscles of the Hand: Median Nerve, Ulnar Nerve, Brachial Plexus, or Small Cerebral Cortical Lesion?

With weakness in the intrinsic muscles of the hand, the cause may be a lesion of the median nerve, ulnar nerve, brachial plexus, or cerebral cortex. Most of the intrinsic muscles of the hand are innervated by the ulnar nerve, so an isolated distal ulnar lesion produces profound loss of use of the hand. This lesion must be differentiated from a lateral frontocentral cerebral lesion, which if located in the hand region produces prominent loss of independent digit use. A median nerve lesion produces impaired hand function because of loss of function of the finger and wrist flexors more than of the intrinsic muscles of the hand. With stabilization of the hand, intact function of ulnar- and radial-innervated muscles can be demonstrated to rule out lesions at or above the plexus.

Lower brachial plexus lesions produce dysfunction of the median- and ulnar-innervated intrinsic muscles of the hand and also may affect the long finger flexors. This dramatic loss of function can be mistaken for central weakness, because the deficit spans peripheral nerve distributions. EMG usually documents the axonal damage.

A small cerebral cortical lesion can produce inability to use the hand, without signs of other deficit. Reflexes should be exaggerated, although acutely they may not be. The combination of cupping of the outstretched hand and pronator drift strongly suggest a central lesion. EMG cannot rule out a peripheral nerve lesion, because several weeks may be required before signs of axonal damage are evident on needle study. MRI of the brain is the most sensitive imaging study for evaluation of a small cerebral lesion.

Weakness of the Wrist: Radial Neuropathy or Small Cerebral Cortical Infarcts?

Radial neuropathy manifests with weakness of the wrist extensors, which if severe can result in destabilization of the intrinsic muscles of the hand and long finger flexors; these median- and ulnar-innervated muscles require opposition from radial-innervated extensors for proper function. Therefore, the deficit seems more extensive than would be expected on the basis of a radial lesion alone. A cerebral lesion is suggested; although cerebral lesions span neural distributions, wrist extension may be more obviously affected than grip or finger flexion.

Differentiation of radial neuropathy from a cerebral lesion depends on demonstration of intact median and ulnar nerve function by the examiner, following stabilization of the finger flexors and wrist. Also, corticospinal tract signs and other signs of cortical damage (aphasia or neglect) should be looked for in a patient with a possible cerebral infarct.

Leg Weakness

Peroneal Nerve Palsy or Paramedian Cerebral Cortical Lesion?

The underlying disorder in leg weakness may be peroneal nerve palsy or a lesion of the paramedian cerebral cortex. Peroneal nerve palsy results in weakness of foot dorsiflexion and eversion, with relative preservation of other motor functions. Small cerebral lesions of the leg region of the homunculus on the medial aspect of hemispheres can cause weakness that is most prominent in the same distribution as for a peroneal nerve palsy. Weakness of foot inversion suggests a cerebral lesion, because this is a tibial nerve function and not expected with peroneal palsy. EMG signs of denervation in the tibialis anterior and other peroneal-innervated muscles indicate a peripheral rather than cerebral lesion. Cerebral lesions producing lower leg weakness usually cause upgoing plantar response and hyperactivity of the Achilles tendon reflex, despite little clinical evidence of gastrocnemius muscle involvement.

Cauda Equina Lesion, Myelopathy, or Paramedian Cerebral Cortical Lesion?

This chapter discusses monoplegia rather than paraplegia (see Chapter 24), but with leg weakness, it is important to differentiate between lower spinal cord dysfunction and cauda equina compression, between upper spinal cord involvement and cervical spondylotic myelopathy, and between these problems and midline cerebral lesions producing leg weakness.

Cauda equina lesions usually are due to acute disc herniations, spondylosis, or tumors in the lumbosacral spinal canal. The lumbar and sacral nerve roots are compressed, resulting initially in a depolarizing block but later axonal degeneration, which produces motor and sensory loss. With the syndromes of intermittent claudication of the cauda equina, repetitive nerve action potentials result in severe pain that is relieved by rest after only a few minutes and that may be accompanied by neurological dysfunction. Pain, sensory loss, and weakness typically are worsened by standing and relieved by flexing the lumbar spine.

Spondylotic myelopathy is compression of the spinal cord by degenerative spondylosis, usually in the cervical region. Compression of the corticospinal tracts produces weakness of the legs. Pain usually is near the level of the lesion, although the localizing value is not precise. Midline cerebral lesions produce unilateral or bilateral leg weakness, depending on the cause and exact location, with CST signs. Spine pain is not expected.

Differentiation among cauda equina, spinal cord, and cortical lesions can be tricky but in general the following rules apply:

Bowel and bladder incontinence can develop with all three locations but is more common with cauda equina lesions.