eMedicine Specialties > Physical Medicine and Rehabilitation > Stroke
Stroke Motor Impairment
Updated: Jul 29, 2008
Introduction
Cerebrovascular disease is the third leading cause of death and the leading cause of disability in the United States. The incidence in the United States is approximately 700,000 cases per year, resulting in an estimated 170,000 fatalities annually. . An estimated 3 million people are living today who have sustained a stroke at some time in the past.
Individuals who have survived a stroke present with varying degrees and types of neurologic impairments and functional deficits. Stroke etiology is divided into ischemic (90%) and hemorrhagic (10%). Of ischemic strokes, the thrombotic type is the most common, followed by embolic and lacunar types, respectively. Strokes are further classified by the brain's anatomic blood supply and related neurologic structures. Each stroke has a varied clinical presentation secondary to vascular anomalies and the size and extent of the lesion.
This article outlines the vascular supply of the brain, anatomic associations, and various clinical presentations observed in stroke as it relates to motor function. Brain stem syndromes also are highlighted, and the anatomical relationships are described. Lastly, stroke motor recovery is discussed, including neurophysiologic and neurotransmitter alterations.
For excellent patient education resources, visit eMedicine's Stroke Center. Also, see eMedicine's patient education article Stroke.
Blood Supply Of The Brain
Understanding the normal function of the brain requires knowledge about the blood supply of the brain. Arterial supply of the brain is derived from 2 pairs of vessels, the internal carotid artery (ICA) and the vertebral artery (VA). The ICA supplies most of the telencephalon and diencephalon, whereas the VA supplies the brain stem, cerebellum, spinal cord, occipital lobe, temporal lobe, and parts of the diencephalon. The ICA travels alongside the optic chiasm and bifurcates into the medial cerebral artery (MCA) and anterior cerebral artery (ACA). Before bifurcation, it gives rise to 2 smaller branches, the anterior choroidal artery and posterior-communicating artery. The anterior choroidal artery supplies the optic tract; choroid plexus; part of the cerebral peduncle; and portions of the internal capsule, thalamus, and hippocampus.
The ACA runs medially, superior to the optic nerve, and enters the longitudinal fissure. Then it follows the corpus callosum supplying the anterior four fifths of the corpus callosum and medial aspect of the frontal and parietal lobes. The ACA then divides into 2 branches, the pericallosal and callosomarginal arteries. Near the entrance into the longitudinal fissure, the anterior communicating artery connects the 2 ACAs. Deep branches, arising near the circle of Willis (proximal or distal to the anterior communicating artery), supply the anterior limb of the internal capsule, the inferior head of the caudate nucleus, and the anterior part of the globus pallidus. The largest of these deep branches is the artery of Heubner. Since parts of the precentral and postcentral gyri extend onto the medial surface of the frontal and parietal lobes, ACA occlusions cause contralateral motor and somatosensory deficits, primarily of the lower extremities.
The MCA proceeds laterally into the lateral sulcus and spreads to supply virtually the entire lateral surface of the cerebral hemisphere, where most of the precentral and postcentral gyri are located. Included in this region is the center for lateral gaze, the motor speech area of Broca, and the sensory language area of Wernicke. The MCA gives rise to many smaller branches (lenticulostriate arteries) that penetrate the brain near their origin and supply deep structures of the diencephalon and telencephalon (cerebral hemisphere). These structures include the putamen, part of the caudate nucleus, the outer globus pallidus, the posterior limb of the internal capsule, and the corona radiata. The MCA is larger than either the ACA or posterior cerebral artery (PCA), and it supplies a larger territory.
The vertebrobasilar system has many variations. The VA is divided into 4 segments.
- The first segment of the VA originates as the first branch of the subclavian artery and enters the costotransverse foramen of C6 or C5.
- The second segment is located entirely within the transverse foramen from C6 through C2.
- The third segment is highly tortuous. This segment emerges from the transverse foramen of C2, then encircles the posterior arch of C2 and passes between the atlas and occiput. This segment is covered by muscle and nerves and is pressed against bone.
- The fourth segment is the only intracranial portion and enters through the foramen magnum.
Then, at the level of the pontomedullary junction, the 2 VAs form the basilar artery (BA). The somewhat smaller BA divides near the pontomesencephalic (pontine-midbrain) junction to form 2 PCAs.
Variations of the VA are common. Sometime the VA-BA junction is higher and the VA supplies the mid pons and lower pons. In about 8% of humans, the VA originates directly from the aortic arch, not the subclavian artery.
Prior to forming the BA, the VA gives rise to 3 branches: the posterior spinal artery, the anterior spinal artery, and the posterior inferior cerebellar artery (PICA). The posterior spinal artery supplies the posterior one third of that half of the spinal cord. The anterior spinal artery supplies the ventral two thirds of the spinal cord. Only one anterior spinal artery forms from a branch from each VA. The PICA supplies the inferior cerebellum, the lateral medulla, and the choroid plexus of the fourth ventricle.
The PICA is the largest branch of the VA and also has many variations. The lateral medulla rarely is fed primarily from the PICA; in most cases, the major blood supply is direct through the lateral medullary branches of the VA. The only part of the medulla that the PICA constantly supplies is the dorsal tegmental area, together with posterior spinal arteries.
The PCAs supply the medial and inferior surfaces of the occipital and temporal lobes. They also send branches to the rostral midbrain and caudal diencephalon and give rise to several posterior choroid arteries, which supply the choroid plexus of the third ventricle. Prior to the division of the BA into the 2 PCAs, the BA gives rise to numerous pontine arteries, the anterior inferior cerebellar artery (AICA), and the superior cerebellar artery (SCA).
The AICA encircles the lower pons and supplies a small ventral surface of the anterior medial cerebellum. In addition, the AICA supplies the lateral pons, including the facial, trigeminal, and vestibular nerves; the cochlear nuclei; the root of the seventh and eighth cranial nerves; and the spinothalamic tract. The SCA encircles the upper pons and supplies the rostral part of the cerebellum, as well as the dentate nucleus. These 3 major arteries (ie, PICA, AICA, SCA) and their branches are connected by numerous free anastomoses that limit infarct size in patients who have cerebellar, VA, or BA occlusion. Major branches of the BA are generally uniform. The small arterial penetrating branches of the VA and BA are even more uniform.
Arterial penetrators have been subdivided into 3 groups. First, the median arteries penetrate the brain stem and supply the paramedian basal and tegmental regions. Second, the short lateral circumferential arteries supply the intermediate tegmental and basal region. Third, the long lateral circumferential arteries supply the lateral basal and tegmental region. The medial tegmental region has a rich collateral blood supply, making it more resistant to ischemia than the base or lateral tegmentum.
The circle of Willis is comprised of the ACA, MCA, PCA, ICA, anterior communicating artery, and posterior communicating artery. The PCA is connected to the ICA by the posterior communicating artery and allows the ACA to communicate with the PCA. Normally, there is little or no blood flow around this circle because the pressure of the right ICA is about the same as that of the right PCA. However, if one major vessel becomes occluded, the communicating arteries may allow critically important anastomotic flow and prevent neurologic damage. Yet, this anastomotic flow depends on the time course of the occlusion. A small communicating artery can enlarge slowly to compensate for a slowly developing occlusion, but an abrupt occlusion might cause serious neurologic damage. Less than one half the circles have this normal construction, with many possible variations.
Asymmetries are common. One or more of the communicating arteries may be very small, one ACA may be smaller than the other, or one PCA may retain its embryologic origin from the ICA and may be connected to the BA through a posterior communicating artery. In rare cases, one of the communicating arteries may be missing, resulting in an incomplete circle. Other routes of collateral circulation exist. Anastomoses are found at the arteriolar and capillary levels between terminal branches of the cerebral arteries.
Stroke Syndromes
MCA stroke
The classic picture of total occlusion is contralateral hemiplegia, hemianesthesia/hyperesthesia, and homonymous hemianopsia, with deviation of the head and eyes toward the side of the lesion. In addition, dominant-hemisphere lesions (usually left) can cause receptive aphasia (inferior division of the MCA to the Wernicke area) and/or expressive aphasia (superior division of the MCA to the Broca area). Gerstmann syndrome consists of asomatognosia (right-left confusion), dyscalculia, finger agnosia, and dysgraphia. Nondominant hemisphere lesions can cause amorphosynthesis (defective perception of sensation from one side of the body), hemineglect, and visuospatial deficits. Insight and judgment are also affected. Greater involvement is noted in the upper extremities and face (central facial paresis) than in the lower extremities. A large infarction may cause local edema, resulting in brain stem compression and loss of consciousness.
The sensory deficit may include impaired position sense, tactile localization, and 2-point discrimination. Stereoanesthesia and graphesthesia may also be seen. Variable changes in touch, pain, and temperature sense also may be experienced. For a more complete review of MCA stroke syndromes, see Middle Cerebral Artery Stroke.
ACA stroke
Occlusion of the ACA proximal to the anterior communicating artery usually is well tolerated (see Blood Supply of the Brain). Maximal disturbance occurs when both arteries arise from one anterior cerebral stem, causing infarction of both medial cerebral hemispheres and resulting in paraplegia, incontinence, abulia and aphasic symptoms, and frontal lobe personality changes. While no universal syndrome exists due to collateral variability, certain phenomena most frequently are associated with ACA stroke.
Complete infarction due to occlusion of one ACA distal to the anterior communicating artery results in sensorimotor deficit of the opposite foot and leg. The arm also may be involved to a lesser degree, while the face and tongue largely are spared. Lesions in the paracentral lobule and upper portion of the motor cortex account for this clinical presentation. In addition, apraxia, mental and personality changes, primitive reflexes, conjugate eye deviation towards the side of the lesion, abulia, and bowel and bladder incontinence often are present.
Generally, the sensorimotor deficits are greater distally, with muscle tone being flaccid initially and then changing to spastic; however, total ACA occlusion, including the recurrent artery of Heubner, results in contralateral hemiplegia with severe paralysis of the face, tongue, and arm, especially the proximal arm. Marked spastic weakness of the distal lower extremity also occurs.
Other disorders include transcortical motor aphasia, alien arm or hand, and disorders of behavior. Transcortical motor aphasia may occur with occlusion of the Heubner branch of the left ACA. Alexander and Schmitt cited a case with right hemiplegia (predominantly in the legs) and right hand and buccofacial apraxia accompanied by a decrease or absence of spontaneous speech, agraphia, and a limited ability to name objects but with a striking preservation of the ability to repeat spoken and written sentences. Disorders of behavior that might be overlooked are abulia (inability to make decisions), slowness and lack of spontaneity, tendency to speak in whispers, and distractibility.
PCA stroke
Patients with PCA stenosis often have transient ischemic attacks (TIAs) alone or immediately preceding infarction. Patients may have symptoms identical to classic migraine attacks with temporary hemianoptic field defects, except they are much more brief and do not progress over minutes like migraine auras. Paresthesias are common, usually of the face and hands, as are transient spells of numbness.
Some patients have reported limb clumsiness, light-headedness, and brief confusion. Repeated pure sensory TIAs that are without visual components and occur over a period of weeks to months rarely are due to PCA disease but are common in patients with pure sensory lacunar infarction. The most common abnormality of unilateral PCA infarction is contralateral visual field defects of hemianopsia, often with macular sparing. In addition, patients may report a grayness, difficulty focusing, bumping into things, or blurred vision.
Dominant hemisphere lesions usually involve language or memory, dyslexia, color anomia, and alexia. Patients who have alexia without agraphia are able to write, speak, and spell normally, but they cannot read words and sentences and cannot name colors. Nondominant PCA lesions can cause prosopagnosia (cannot recognize familiar faces).
Visual perception in the right visual cortex is not believed to reach the language zone in the left temporal-parietal region. Because the left language area is not damaged, writing, speaking, and spelling are preserved. These nonvisual aspects probably cross the corpus callosum more anterior to the PCA infarct. When agraphia is present, reading, writing, and spelling all are abnormal, and infarction usually involves the angular gyrus region.
Bilateral PCA infarct as a result of BA occlusion presents with cortical blindness due to bilateral infarction of the striate cortex. Bilateral hemianopsia with sparing of parts of the visual field, intact pupillary reflexes, and Korsakoff amnesia is common.
Anton syndrome
Anton syndrome, occasionally known as Anton-Babinski syndrome, is a form of cortical blindness in which the patient denies the visual impairment. Anton syndrome is caused by damage to the occipital lobe, which extends from the primary visual cortex into the visual association cortex.
Lacunar Infarcts
Lacunes are the single most common lesions found in the brain stem. They are found most commonly in the pons and thalamus, but they do occur in the medulla and midbrain. At postmortem, lacunes tend to be multiple, even though the term is reserved for infarctions within the territory of a single perforating artery. Many lacunar infarcts present as a slight deficit that is impossible to distinguish from an incomplete stroke because of large vessel disease or embolism. Additionally, as many as 80% of lacunar infarcts are clinically silent. The classic literature includes descriptions of 5 syndromes produced by lacunar infarcts.
- Pure motor hemiplegia syndrome
- The lesion is typically in the posterior limb of the internal capsule. Fisher and Curry defined this syndrome as a complete or incomplete paralysis of the face, arm, and leg on one side of the body without sensory signs, visual field defects, dysphasia, or deficits of higher cognitive function or apractagnosia. In addition, the hemiplegia is free of vertigo, deafness, tinnitus, diplopia, cerebellar ataxia, and gross nystagmus. This definition applies to the acute phase of vascular insult and does not include less recent strokes in which other signs were present initially but faded with the passage of time. The complete syndrome is somewhat uncommon.
- As a clinical rule, such a diagnosis applies when the affected side involves one part more than the other. Pure motor stroke has been reported from autopsied cases with focal infarction involving many different areas of the brain stem. The most frequent correlation has been with capsular lesions, especially the posterior limb. Posterior limb capsular lacunes usually involve the pallidum and posterior limb of the capsule, which are supplied by the lenticulostriate branches of the MCA.
- Pure sensory syndrome
- A lacunar infarction in the somatosensory nuclei of the thalamus, ventral nuclei (posterior lateral and posterior medial nuclei), and parietal white matter produces sensory symptoms on the opposite side of the body and face without motor, cerebellar, or higher cortical function abnormalities. Paresthesias usually are present in at least 2 different parts of the body (eg, face and arm, arm and leg).
- Limbs often are involved more than the face, but sometimes the chest and abdomen also are involved. When the hand is involved, all the digits usually are affected. The symptoms of sensory dysfunction usually far exceed the objective signs, which may be normal. Patients may have only proprioceptive loss with intact pain and temperature sensation.
- Sensorimotor syndrome
- A lacunar infarct may involve both thalamic sensory nuclei and the adjacent posterior limb of the internal capsule, leading to hemiparesis, pyramidal signs, and hemisensory loss on the contralateral side, without visual or intellectual dysfunction.
- This syndrome is very difficult to differentiate from large vessel disease. Neurologic deficits usually develop over a period of hours to a few days and rarely evolve over more than 7 days. Usually, headaches do not accompany the symptoms, and the patient remains alert. A past medical history of hypertension and/or diabetes also may help to distinguish this syndrome from large vessel disease.
- Ataxia hemiparesis
- Ataxia hemiparesis has both cerebellar and pyramidal elements. This condition initially was described as homolateral ataxia with crural paresis, its most familiar form. Although the syndrome typically results from infarction, usually of the rostral pons, it has been reported to result from tumor or intracerebral hemorrhage in the parasagittal part of the precentral area. Ataxia hemiparesis resulting from the latter 2 causes does not present in as pure of a form as does ataxia hemiparesis resulting from infarction.
- Clinical features present as mild-to-moderate weakness of the legs, especially the ankles, with little or no weakness of the upper limbs and face. Ataxia of the arm and leg on the same side also occurs. In a few cases, a mild and transient hemisensory deficit initially may accompany the motor findings. Similar to the other lacunar syndromes, this syndrome changes, with the hemiparesis resolving and the ataxia remaining. In all cases, the degree of ataxia is more striking than the weakness and exceeds that attributable to weakness alone.
- Dysarthria clumsy-hand syndrome
- Lesion is at the basis pontis. For patients presenting with this syndrome, the dysarthria and the ataxia of the upper limb appear to be the prominent components of the clinical deficit, but they do not occur in isolation. The syndrome also includes facial weakness (which may be profound), dysphagia, and some degree of weakness of the hand and even the leg. The reflexes of the affected side usually are exaggerated and the plantar response is extensor. The clinical picture usually develops suddenly.
- The cardinal features of this syndrome are moderate-to-severe dysarthria, corticobulbar weakness of the lower face and tongue, and slowness of fine motor movements of one hand. The best-recognized association has been with lacunes of the anterior limb of the internal capsule. In a few other cases, the lesion has been in the basis pontis. The syndrome also has been reported from hemorrhage of the pons. The outlook for functional recovery from this syndrome is good.
Brain Stem Stroke Syndromes
The sine qua non of VA-BA stroke syndromes is sensory or motor abnormalities that are bilateral or crossed coupled with unilateral or bilateral cranial nerve deficits scattered from cranial nerves (CNs) III-XII. Other common findings include abrupt onset of headache, dizziness, impaired awareness, diplopia, nystagmus, strabismus, nausea, emesis, incoordination, vertigo, dysarthria, dysphagia, other bulbar or pseudobulbar signs, homonymous hemianopsia, blindness, visual agnosia, or pyramidal tract signs. For further information, see Vertebrobasilar Stroke.
Lateral medullary syndrome
Of all the brain stem syndromes, the lateral medullary syndrome, also known as Wallenberg syndrome, is the best known and most studied. In 1895, Wallenberg injected autopsied brains and concluded the PICA should be occluded to establish the diagnosis of lateral medullary infarct (LMI). Fisher and colleagues and Escourolle and colleagues demonstrated that not one artery but several small arteries from the VA usually supply the lateral medullary area. In fact, the PICA participates in the supply of the lateral medullary in less than one third of cases. Today, it is known that the main supply to the lateral medullary area is from direct penetrating arteries of the distal VA, hence the VA system is the most common location of vascular lesion in patients with LMI.
The VA is occluded in approximately 75% of cases. VA occlusions are thrombotic in 75% of cases; the remainder of cases are due to cardiac embolism. Small branches of the AICA and BA also supply the lateral medullary area variably. Of note, when the PICA or AICA is involved, patients usually have cerebellar symptoms due to cerebellar infarct. With PICA occlusion or infarction, major signs include gait and trunk ataxia, ipsilateral axial lateropulsion, or both. The presence of these signs usually prevents the patient from standing in the upright position. Thus, patients able to stand or walk with a tandem gait are unlikely to have a significant cerebellar infarct.
Symptoms of lateral medullary syndrome consist of vertigo, headache, facial pain, dysequilibrium, nausea and vomiting, ataxia, hiccups, and contralateral burning pain. Vertigo usually is characterized by dizziness with staggering gait and double vision, which occur gradually, in a step-wise progression over 24-48 hours. Vertigo is unusual after 2 weeks.
Facial pain is more diagnostic, as it presents ipsilateral to the lesion and is sharp and stabbing, with jolts of pain most commonly in the eye as well as in the face. The patient may have contralateral loss of pain and temperature sensation or may experience burning pain in the face. Facial pain often is the first symptom perceived at the onset of stroke, probably because of the descending tract of CN V. Hence, patients must be questioned regarding these symptoms.
With dysequilibrium, the patient has the sensation of swaying or falling and may describe this sensation as feeling seasick. Patients may have visual dysfunction and diplopia related to vestibular nerve involvement. Yet, extraocular muscles, visual fields, and visual acuity remain intact.
Ataxia is the rule, not the exception. All patients with LMI have abnormal gait. Ataxia of gait is the most frequent symptom at onset, and it can be severe enough to prevent sitting or standing. Patients may report weakness when they really are experiencing clumsiness.
Difficulty swallowing, hoarseness, and dysarthria are additional symptoms. Difficulty swallowing has been related to dyscoordination of the epiglottic closure, palate, and pharynx due to a central lesion in the nucleus ambiguus. Food gets stuck in the piriform recess of the pharynx adjacent to the larynx; patients attempt to extricate the material by an unusual coughlike maneuver. This cough, which sounds like crowing, is characteristic and, in an individual who has had a stroke, is virtually diagnostic of LMI.
Signs of lateral medullary syndrome include sensory deficits of pain and temperature on the ipsilateral face and contralateral body, ipsilateral Horner syndrome (often incomplete, with ptosis and miosis most common), ataxia, nystagmus, and paralysis of the ipsilateral vocal cord and palate. Many clinicians believe paralysis of the ipsilateral vocal cord and palate due to a lesion in the nucleus ambiguus unequivocally localizes the infarct to the lateral medullary region. On the other hand, contralateral hemiparesis or the Babinski sign are not components of lateral medullary infarction and indicate a wider, more medial, zone of ischemia.
Ataxia may be of both gait and limb. Limb ataxia (dysmetria) is ipsilateral and often is confused with weakness. If the PICA territory is involved with infarct of the inferior cerebellum, then leaning, veering, falling, or toppling to the side when erect or sitting is present. This deficit usually subsides, leaving only minor clumsiness at 3-6 months after the stroke.
Nystagmus usually is horizontal or rotary; it is rarely vertical. On examination, patients have small quick nystagmus on voluntary gaze to the contralateral side and coarse large amplitude with slower nystagmus on the ipsilateral gaze. Some patients may have forcibly deviated eyes to the side of the lesion and may demonstrate lateropulsion (eyes may drift away from the side of the lesion) due to the vestibular-ocular reflex.
Case reports have documented occurrences of dysfunction of the autonomic system (unexplained tachycardia or blood pressure control) and respiratory regulation (sleep apnea, Ondine curse) in patients with LMI. Such abnormalities may occur more commonly than they are clinically recognized.
Medial medullary syndrome
The full medial medullary syndrome consists of upper and lower limb hemiplegia (face spared) and loss of posterior column sensation (position and vibration) on the contralateral side and involvement of the tongue on the ipsilateral side due to involvement of the corticospinal tract at the medullary pyramid, the lateral lemniscus, and hypoglossal nucleus or nerve. However, some patients may lack tongue or posterior column sensory loss and may present with pure motor hemiparesis. The anatomic basis for the crossed hemiplegia is infarction of the medullary pyramid, a region supplied by the anterior spinal artery. Occasionally, the hemiparesis is ipsilateral to the infarct and is due to infarction of the pyramid more caudal in the lower medulla and rostral spinal cord after the pyramidal decussation.
Medial medullary syndrome is very rare. Paramedian arteries supplying the medial medullary territory arise from the anterior spinal arteries, which are branches of the VA. Each VA gives rise to one or several small paramedian anterior spinal branches, which join to form the anterior spinal artery. This anatomy usually prevents spinal cord or medial medullary infarction in the case of unilateral VA occlusion. In a postmortem analysis of medullary infarction, 7 of 10 medial infarcts were due to blocking of the anterior spinal artery branch by occlusion of the distal intracranial VA.
Medial medullary infarcts are seldom single. More often, the medial medullary syndrome is seen combined with the lateral medullary syndrome, forming a hemimedullary infarction or Babinski-Nageotte syndrome. Occasionally, the hemiparesis is ipsilateral to the infarct, is on the side of cerebellar signs, and is contralateral to pain loss. The anatomic explanation for the characteristics of these symptoms is infarction of the pyramid more caudal in the lower medulla and rostral spinal cord after the pyramidal decussation. The combined syndrome invariably is caused by VA occlusion.
Nearly 50% of all reported cases of medial medullary infarction are bilateral. Flaccid or spastic quadriparesis and impaired control of respiration have been the most consistent clinical findings in patients with bilateral medullary infarctions. These signs and symptoms follow a step-wise progression over several days, with severe paresis and the risk of death usually remaining because of respiratory and circulatory abnormalities.
Uncommon Classic Brain Stem Syndromes
Millard-Gubler syndrome
The Millard-Gubler syndrome is described as an alternating hemiparesis with ipsilateral lateral rectus and facial palsy and contralateral upper and lower limb hemiparesis due to damage of the CN VI tract, the CN VII tract, and the corticospinal tract. A facial palsy can occur independently of a CN VI palsy when the lesion is more lateral (low pons base). The ipsilateral facial palsy is of the lower motor neuron type, involving the forehead, eyelids, and eyebrows. This syndrome is most consistent with a ventral paramedian pontine lesion.
Foville syndrome
The Foville syndrome is another alternating hemiparesis syndrome. This syndrome usually results when the lesion is located in the low pontine tegmentum (paramedian pontine reticular formation). Patients with this syndrome have nuclear CN VII paralysis on the same side as a conjugated lateral (horizontal) gaze palsy (toward the side of the lesion) and a crossed hemiparesis. The entire ipsilateral face is involved. When the patient is attempting to look ipsilateral to the lesion, either conjugately or with either eye alone, the globes move only as far as the midline. Clinically, the only way to distinguish Millard-Gubler syndrome from Foville syndrome is the absence or presence of lateral gaze palsy, respectively.
Weber syndrome
This syndrome is the third and most superior alternating hemiparesis. This rare type of ventral midbrain lesion involves the crus cerebri (corticospinal and corticobulbar tracts) and CN III. Patients display ipsilateral oculomotor paralysis with contralateral hemiparesis. The affected eye is dilated with negligible response to light or accommodation, and it has ipsilateral ptosis and external strabismus. The affected eye usually is motionless, except for lateral gaze, which is reduced. Some patients still may have abduction, internal rotation, and depression due to the intact CN IV. Sometimes, ipsilateral ptosis may mask the initial diplopia.
Benedict syndrome
This midbrain syndrome affects CN III (ie, oculomotor nerve), the red nucleus, and the cerebral peduncle, resulting in contralateral hemiparesis with tremor in the paretic limb and ipsilateral oculomotor palsy. Oculomotor deficits include ptosis, external strabismus, and a dilated pupil. The red nucleus coordinates cerebellar thalamic fiber tracts to the superior cerebellar peduncle (brachium conjunctivum). A lesion in the red nucleus (upper part) results in a contralateral coordination deficit (ataxia), dysmetria, dysdiadochokinesia, rubral tremor (coarse resting tremor that increases with movement), and pseudo-Parkinson tremor. Sometimes, this syndrome affects the medial lemniscus or spinothalamic tract, with contralateral sensory deficits of (1) light touch and proprioception and (2) pain and temperature, respectively. In many ways, this syndrome can be considered to be a combination of the Weber syndrome and the Claude syndrome.
Claude syndrome
This syndrome affects the midbrain and involves CN III and the lower part of the red nucleus. Patients develop ipsilateral CN III palsy with contralateral ataxia and limb dysmetria. The physical findings are very similar to those in Benedict syndrome, without the hemiparesis. Thus, depending on the midbrain territory involved, a spectrum of CN III palsy and contralateral hemiparesis and/or tremor and ataxia usually are seen.
Parinaud syndrome
This syndrome is the result of a lesion in the rostral midbrain that leads to the superior colliculus, thus affecting the pretectal nuclei (high midbrain ventral to superior colliculus) and corticotectal fibers (supranuclear fibers to CN III). Clinically, patients with Parinaud syndrome demonstrate paralysis of upward conjugate gaze, convergence, and pupillary areflexia. Paralysis also is seen when each eye is tested separately, and, frequently, there is a downward conjugate palsy. Pupillary abnormalities and other ocular signs may be present. Horizontal movements are normal.
Jackson syndrome
Patients with Jackson syndrome present with unilateral weakness or paralysis of structures innervated by the vagus nerve (ie, CN X), the spinal accessory nerve (ie, CN XI), or the hypoglossal nerve (ie, CN XII). CN X supplies the ipsilateral soft palate, pharynx, and larynx. CN XI supplies the ipsilateral sternocleidomastoid (SCM) and trapezius muscles, while CN XII supplies the ipsilateral tongue. Signs and symptoms include hoarseness and dysphagia, as well as unilateral weakness and atrophy of the soft palate, trapezius, SCM, and tongue.
Locked-in syndrome
In 1966, Plum and Posner coined the term locked-in syndrome (LIS) to describe a state in which severe paralysis prevents the usual means of gestural and vocal communication. The classic criteria are paralysis of all cranial nerves (except those for vertical eye movements), tetraplegia, and preserved consciousness. LIS usually is due to bilateral pontine (base) infarction related to the BA thrombosis or bilateral occlusion of paramedian arteries. Occasionally, it can be due to bilateral midbrain infarction.
Kemper and Romanul described a patient who, although totally paralyzed and speechless, could move his eyes horizontally and raise his eyebrows. Kemper and Romanul sought to differentiate this condition from akinetic mutism, a condition in which the patient could, under certain circumstances, speak and move.
In LIS, the patient usually can communicate by vertical eye movements or blinking and can demonstrate comprehension of the circumstance and environment. Some individuals with LIS have oral automatisms, in the form of chewing and sucking, that can be induced by oral or perioral stimulation, indicating loss of voluntary control over bulbar masticatory function.
Pseudobulbar palsy
This syndrome is characterized by dysarthria, dysphagia, dysphonia, impairment of voluntary movements of the tongue and facial muscles, and emotional lability. This condition is caused by lesions that affect the motor fibers that travel from the cerebral cortex to the lower brain stem (ie, corticobulbar tracts).
Motor Recovery From Stroke
Cerebral vascular disease affects approximately 700,000 individuals in the United States annually, with a 20% initial mortality rate, thus leaving approximately 400,000 stroke survivors annually. It is the third leading cause of death and the leading cause of disability in the United States. Most stroke recovery occurs in the first 2-3 months. At 2-3 years, greater than 90% of recovery has occurred. Recovery can continue for many years. Measures of functional recovery at 1 year poststroke include that 75-85% of patients are ambulatory, 48-58% regain independence in performance of activities of daily living (ADL), and 10-29% require nursing home care.
Various clinical factors consistently have been associated with less favorable outcomes, which are defined as lower discharge functional status and/or nursing home placement after inpatient rehabilitation. These factors include medical comorbidities (eg, diabetes mellitus [DM], cardiac disease, ECG abnormalities), prior stroke, prior functional dependence, neglect, sensory and visual deficits, severe motor deficits, loss of consciousness (LOC), cognitive deficits, and incontinence.
Recovery is the most rapid in the first 3 months following stroke, but continued improvement often is seen beyond the first year. Motor recovery tends to reach plateau more quickly than functional recovery, with little change seen after 8-12 weeks. Recovery of arm movement is less complete than recovery of leg movement, perhaps because arm paresis usually is greater than leg paresis and because the arm requires finer movements to perform skilled activities. The lack of initial movement or measurable grip strength by 4 weeks following onset is associated with a less favorable prognosis for return of useful arm function.
The following several observations have emerged in the natural history of stroke recovery:
- Motor recovery usually occurs in a predictable pattern, and the patient tends to reach a plateau after 3 months. However, recovery can continue, at a slower pace, for many years.
- Functional recovery generally continues to improve for 6 months to 1 year following stroke.
- Some patients continue to improve for several years following stroke and show remarkable and unexpected recovery.
- Recovery can occur in spite of extensive CNS damage and advanced age.
Language does not improve evenly across all components. In most studies, comprehension skills demonstrate the best recovery. The different types of aphasia also have differing prognoses for recovery; the worst is global aphasia (usually 6 mo to 1 y), and the best is anomic aphasia. Recovery from aphasia appears to occur independently of recovery from hemiparesis.
Neurophysiologic mechanisms for recovery from stroke
The neurophysiology of stroke recovery is not fully understood. Recovery often is attributable to the resolution of edema and return of circulation to the ischemic penumbra; however, as noted by Brodal, these mechanisms cannot account for recovery occurring beyond 4-6 weeks following stroke.
There a many factors can contribute to brain reorganization after stroke, including improved synaptic transmission, loss of perilesional GABA-ergic inhibition, increased glutamatergic activity, changes in neuronal-membrane excitability, and removal of inhibition. Additionally, numerous alterations in neurotransmitters and cerebral metabolism occur following brain injury. These modifications contribute to the observed deficits via action, both at the site of injury and in remote areas of the brain. Collectively, these mechanisms give rise to the concept of neuroplasticity.
The concept of neuroplasticity includes all possible mechanisms of neuronal reorganization, including recruitment of pathways that are functionally similar to, but functionally different from the ischemic ones, synaptogenesis, dendritic arborization, and reinforcement of existing but functionally silent synaptic connections.
Several clinical observations illustrate the bilaterality of the brain. Perhaps the most dramatic of these observations are the reports of remarkable return of function following hemispherectomy. Papanicolaou demonstrated greater right hemisphere activity in a recovering aphasic patient, as compared to controls. He concluded that the right hemisphere was taking over some of the language function of the damaged left hemisphere.
Cortical reorganization through synaptogenesis and unmasking (formation of new synapses and release from inhibition, respectively) may account for a considerable portion of the recovery seen following stroke. This reorganization may occur both locally and remotely from the lesion. Immediate reorganization may take place through unmasking of previously inactive synapses, a process thought to take place through disinhibition, through the development of denervation hypersensitivity, or by rerouting of impulse traffic as a result of a rapidly acting feedback mechanism. The slower recovery may be explained by axonal or dendritic sprouting.
Many reports document the ability of CNS neurons to sprout; however, neuronal sprouting and synaptogenesis can be maladaptive, leading to spasticity, memory dysfunction, and seizures. Evidence suggests that dendritic development depends on repetitive functional demand or training in specific activities. Early training may be particularly beneficial.
Alternatively, the redevelopment of adequate inhibition following stroke may play an important role in recovery. Mass movements and pathologic reflexes reflect a loss of inhibitory mechanisms. Creutfeldt emphasized the importance of inhibition. He noted that each cortical neuron is inhibited by its neighbor and that the descending influence of the cortex is predominantly inhibitory. The development of inhibition may be responsible for the reappearance of fine coordinated movements.
Neurotransmitter alterations
Multiple changes in neurotransmitters take place over varying time frames, and some may be directly responsible for or associated with the observed decrease in brain metabolism and function. The following drug classes are thought to have a positive effect on motor recovery: cholinergic and anticholinesterases, norepinephrine, amphetamines, L-dopa, and phenylpropanolamine. Phenylpropanolamine has been recalled from the US market. Conversely, drugs that antagonize the norepinephrine system (eg, haloperidol, phenoxybenzamine) have been shown to retard recovery of motor function when given early after injury. In addition, drugs commonly prescribed following stroke (eg, benzodiazepines, anticonvulsants, alpha-blocking antihypertensives) also may interfere with recovery. Gamma-aminobutyric acid (GABA) and serotonin are major inhibitory transmitters in the CNS. Levels of both are elevated following brain ischemia.
Drugs that enhance GABA-ergic transmission disrupt recovery after brain injury. Experimental studies show that benzodiazepines, phenytoin, and barbiturates are harmful when given during the recovery period; however, several studies have shown that early GABA-ergic activation improves stroke outcomes and that benzodiazepine use just before stroke may have potentially positive effects on reperfusion after an embolic infarct. Thus, for GABA-ergic agents, the timing of administration in relationship to the ischemic event may be a critical determinant of whether a drug has a beneficial or harmful effect. Goldstein et al suggest that alpha2-adrenergic receptor agonists are harmful; whereas, alpha2-adrenergic receptor antagonists, which increase the rate of firing of central noradrenergic neurons by blocking autoreceptors, are beneficial during recovery.
Conclusion
Stroke syndromes present with various alterations in motor, sensory, and cognitive function, each unique in clinical presentation and prognosis. Although there are general principles of stroke recovery, no two patients share the same experience. Understanding the correlated physiologic and anatomic changes in the brain helps identify which syndrome is present and how best to institute comprehensive rehabilitation to meet the individual needs of the patient.
Keywords
stroke syndromes, lacunar infarcts, brainstem stroke syndromes
Christopher J Godbout, MD, Consulting Staff, Nash Regional Pain Center, Nash Health Care Systems, and Jeffery S Johns, MD, Associate Hospital Medical Director, Medical Director of Spinal Cord Injury Program, Brooks Rehabiliation Hospital; Adjunct Clinical Assistant Professor, Department of Physical Medicine and Rehabilitation, University of North Carolina School of Medicine, contributed to this article.
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Further Reading
Keywords
stroke syndromes, lacunar infarcts, brainstem stroke syndromes
