Hemiplegia and Monoplegia

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Chapter 23 Hemiplegia and Monoplegia

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.


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.

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.


Both cortical and subcortical infarctions can produce weakness, but cortical infarctions are more likely than subcortical infarctions to be associated with sensory deficits. Also, many cortical infarctions are associated with what is called a cortical sign—neglect with nondominant hemisphere lesions and aphasia with dominant hemisphere lesions. Unfortunately, this distinction is not absolute because subcortical lesions also occasionally can produce these signs.

Initial diagnosis of infarction usually is made on clinical grounds. The abrupt onset of the deficit is typical. Weakness that progresses over several days is unlikely to be caused by infarction, although some infarcts can show worsening for a few days after onset. Progression over days suggests demyelinating disease or infection. Progression over weeks suggests a mass lesion such as tumor or abscess. Progression over seconds to minutes in a marching fashion suggests either epilepsy or migraine; not all migraine-associated deficits are associated with concurrent or subsequent headache.

Computed tomography (CT) scans often do not show infarction for up to 3 days after the event but are performed emergently to rule out mass lesion or hemorrhage. Small infarctions may never be seen on CT. Magnetic resonance imaging (MRI) is superior in showing both old and new infarctions; diffusion-weighted imaging (DWI) on MRI distinguishes recent infarction from old lesions.

Subcortical Lesions

Subcortical lesions are more likely to produce equal weakness of the contralateral face, arm, and leg (hemiplegia) than cortical lesions because of the convergence of the descending axons in the internal capsule. The compact nature of the internal capsule makes it the most likely location for a hemiplegia. The internal capsule is a particularly common location for lacunar infarctions and also can be affected by hemorrhage in the adjacent basal ganglia or thalamus. Weakness of sudden onset is most likely to be the result of infarction, with hemorrhage in a minority of cases. Demyelinating disease is characterized by a subacute onset. Tumors are associated with a slower onset of deficit and can get quite large in subcortical regions before the patient presents for medical attention.

Demyelinating Disease

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

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.


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.

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.

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:

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:

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

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Named Disorder Lesion Location Signs
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