Acute hemiplegia in childhood …

Stroke & Vascular Disorders

Updated 02.20.2026
Released 06.19.1995
Expires For CME 02.20.2029

Acute hemiplegia in childhood

Authors: Haluk Topaloglu MD, Hatice Bektaş MD

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Editor: Nina F Schor MD PhD

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Acute hemiplegia in childhood

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Introduction

Overview

Acute hemiplegia in childhood is a diagnostic and management challenge for the clinician. Hemiplegia is a total paralysis of the arm, leg, and sometimes the face on one side of the body, whereas hemiparesis is partial paralysis on one side. Hemiplegia/hemiparesis is not a disease but a response of the central nervous system to various insults. Underlying etiologies are more diverse in children than in adults. This review is a clinical approach to a child with acute hemiplegia. It includes a staged approach toward clinical assessment, diagnostic workup, and management of specific causes of hemiplegia.

Key points

	• Acute hemiplegia in children is a clinical syndrome with various causes.
	• The immediate priority is to exclude a neurosurgical condition like intracranial hemorrhage, brain tumor, hydrocephalus, and massive ischemic stroke.
	• Acute hemiplegia in children is the most common presentation of vascular stroke syndromes.
	• About 20% to 30% of children with acute hemiplegia have “stroke mimics” like hemiplegic migraine, alternating hemiplegia, Todd paralysis, reversible vasoconstriction syndrome, posterior reversible encephalopathy, and conversion disorder.
	• Clinical data and neuroimaging help to establish the diagnosis in most cases.
	• Management and prognosis of acute hemiplegia in children depend on the etiology.

Historical note and terminology

The occurrence of unilateral weakness related to contralateral brain injury was already familiar to ancient physicians like Hippocrates and Aretaeus. Jusepe Ribera, a 17th century Spanish artist, painted a portrait of young soldier with hemiplegia. Early observations of acute hemiplegia were based on experience with penetrating head injury, intracranial hemorrhage, and epileptic seizures. In the late 18th century, Darwin experimented with electrical therapy for children with hemiplegia (45). Todd described post-epileptic hemiplegia in 1865 (97), and in 1887 Freud described acute childhood hemiplegia associated with epilepsy (75). In 1916, Higier described hemiplegic seizures (52). Seminal papers by Bickerstaff (10), Aicardi and colleagues (02), and Carter (89; 53) focused mainly on childhood stroke and heralded the modern approach to evaluating acute childhood hemiplegia, caused by stroke. The past decade (2015–2025) has witnessed transformative advances in pediatric stroke care. The International Pediatric Stroke Study (IPSS), which began in 2003, has now enrolled thousands of patients across 100 institutions in 34 countries, generating many publications that have fundamentally shaped contemporary practice (61; 40). In addition, structural and functional brain MRI, and traditional and MR angiography, have contributed to our understanding of the multiple causes and pathophysiology of acute hemiplegia in childhood. Advances in next-generation sequencing have accelerated discovery of genetic etiologies, particularly in recurrent childhood stroke and monogenic cerebral vasculopathies (48), expanding our understanding beyond the classical mutations in CACNA1A and ATP1A3 associated with familial hemiplegic migraine and alternating hemiplegia of childhood.

Clinical manifestations

Presentation and course

Clinical manifestations, course, and outcome of acute hemiplegia vary depending on the etiology.

Stroke. Acute hemiplegia, a common presentation of arterial ischemic stroke (65; 43), appears suddenly in 50% of cases but is subacute (evolving over hours) in 35% and stuttering in onset in 15% (32). Arteriopathy in contrast to other causes of stroke almost always presents with hemiparesis as opposed to multifocal or bilateral symptoms (62). Subacute onset also suggests an underlying arteriopathy (12). Duration of hemiplegia varies from days to weeks; deficits can be permanent. Clinical presentation depends on the age, type of stroke, and etiology. Seizures and headaches may precede, present with, or follow arterial ischemic stroke in as many as a third of patients or more (15; 50; 01; 88) and may delay the proper diagnosis (86). Seizures are particularly common in children younger than 1 year of age who may or may not have an apparent hemiparesis (64). Other neurologic signs can co-occur with hemiplegia, eg, hemisensory or visual deficit, aphasia, or constructional apraxia, depending on the location and type of the lesion. Acute hemiparesis is often accompanied by altered consciousness, headache, and seizures in cerebral venous sinus thrombosis with associated infarction and hemorrhagic stroke. Predisposing conditions, eg, dehydration and systemic diseases, are common (27).

Hemorrhage. Hemorrhage can occur in the setting of stroke (arterial or venous), vascular malformations and aneurysms, neoplasms, congenital heart disease, head and neck trauma, and hematologic disorders. Hemiplegia is generally abrupt in onset, except when it occurs in the setting of hemorrhagic stroke. Headaches and seizures are common (60; 15). The clinical presentation may be nonspecific in younger children, whereas in older children (over 6 years of age), a focal deficit or hemiplegia is the rule (60).

Hemiplegic migraine. Hemiplegic migraine usually has a slowly progressive onset evolving over 5 to 30 minutes, but in 5% to 10% of cases, onset is abrupt, peaking in less than 1 minute (26). In about 15%, the hemiplegia shifts sides during an attack. Weakness lasts less than 1 hour in 51% of cases, 1 to 24 hours in a subsequent 41%, and more than 24 hours in an additional 8% (96). In hemiplegic migraine, positive symptoms (particularly paresthesias) often precede the hemiplegia (46), and more typical auras (visual, sensory, or dysphasic) co-occur with the hemiplegia. Headache can precede or occur at the same time as the aura or follow it–generally within an hour. A structural lesion needs to be ruled out as both arterial ischemic stroke and cerebral venous sinus thrombosis occur in migraineurs, at least in adulthood, at a greater frequency than in the general population, and headaches, especially in children, can occur at the onset of stroke. It is not known whether prolonged aura (more than 1 hour but less than 7 days) or persistent aura (more than 7 days) increases the risk for stroke. However, hemiplegic migraine does not specifically confer a greater risk of stroke than migraines with other auras (56).

Seizures: ictal and Todd paralysis. Todd paralysis is identified by its context; it occurs after a seizure. Duration ranges from minutes to days but in most instances is less than 30 minutes (41). Hemiplegia lasting more than 6 hours is unusual and should not be assumed to be a Todd paralysis (46). However, Todd himself reported episodes lasting for days (97). Rarely, focal weakness may be the only manifestation of a seizure (74; 73). A hemiconvulsion-hemiplegia-epilepsy syndrome has been described and is characterized by a prolonged clonic seizure with unilateral predominance occurring during a febrile illness and followed by hemiplegia (06).

Demyelinating disorders. The onset of hemiplegia in disorders affecting white matter, such as acute disseminated encephalomyelitis and leukoencephalopathy due to toxin or medication side effects, is more often subacute than acute and is often associated with an encephalopathy.

Functional neurologic disorder. In functional neurologic disorder, the hemiplegia usually appears suddenly and is typically temporally related to a psychological stressor (04). Other psychiatric disorders (ie, depression and anxiety) may coexist.

Diabetes mellitus. Acute transitory attacks occur in children with insulin-dependent diabetes mellitus. Attacks frequently occur during sleep. Hemiparesis is present on awakening and lasts for 3 to 24 hours. Weakness is greater in the face and arm. Headache is a constant feature. Recovery is complete (34).

Alternating hemiplegia of childhood. Onset is from birth to 18 months. Mild developmental delay and paroxysmal abnormal eye movements (nystagmus, strabismus) are initial features (69). The clinical presentation varies with age: young infants have more dystonic features, and older children have flaccid hemiplegia. Episodes are characterized by abrupt onset of weakness, typically involving the arm more than the leg, lasting from minutes to days. Brief attacks of monocular or binocular nystagmus frequently accompany or precede hemiplegic episodes. The duration of attacks varies from minutes to days. Hemiplegia may shift from side to side. A pathognomonic feature is complete resolution of hemiplegia with sleep, with symptoms resuming on awakening. Neurologic impairment occurs as the disease progresses (94). Adults with this disorder can have other manifestations, including parkinsonism (see MedLink Neurology article Alternating hemiplegia of childhood).

Meningitis or meningoencephalitis. The clinical manifestations of CNS infection differ between the meningitic form and the encephalitic form. Fever, headache, vomiting, and stiffness of the neck dominate the meningitic form, and altered state of consciousness, focal neurologic signs (including hemiplegia), and seizures dominate the encephalitic form.

Reversible cerebral vasoconstriction syndrome. Reversible cerebral vasoconstriction (RCVS) is well-recognized in adults but remains rare in pediatric populations (63). RCVS is a clinical and radiographic syndrome that is characterized by severe, sudden-onset thunderclap headaches with peak intensity typically reached within 1 minute, accompanied by multifocal, segmental vasoconstriction of cerebral arteries that resolves spontaneously within 12 weeks. In children, the clinical presentation may include seizures (21%), focal neurologic deficits, including hemiplegia, and altered mental status. Reversible cerebral vasoconstriction syndrome is associated with stroke (ischemic or hemorrhagic) in 10% of cases. Hypertension is common but not universal. It is frequently associated with ingestion of vasoactive drugs, such as nasal decongestants (79).

Posterior reversible encephalopathy syndrome. Posterior reversible encephalopathy syndrome (PRES) is a neurologic disease characterized by headache, altered mental status, visual disturbance, seizures, and focal neurologic findings, including hemiplegia (47). The syndrome occurs in the setting of acute hypertension, though normotensive PRES is well-described, particularly in children. Common predisposing conditions include renal disease (most common), hematologic malignancies and their treatments (cytotoxic chemotherapy, calcineurin inhibitors, corticosteroids), hematopoietic stem cell or solid organ transplantation, autoimmune disorders (systemic lupus erythematosus, IgA vasculitis), and immunosuppressive therapies. When it is managed in a timely fashion, the prognosis is benign with complete recovery within days or weeks. Typical radiographic findings include vasogenic edema in posterior cerebral regions, though atypical patterns involving frontal lobes, basal ganglia, brainstem, and cerebellum occur in up to 61% to 82% of pediatric cases (17).

Metabolic or genetic disorders. Metabolic abnormalities such as hyper- and hypoglycemia and hypocalcemia result in inadequate energy supply to neurons. Inherited metabolic disorders can cause stroke-like episodes with hemiplegia, which are mediated by cellular energy failure, for example, in mitochondrial disorders like MELAS (mitochondrial encephalopathy and lactic acidosis syndrome) and organic acidemias. Disease-specific mechanisms for stroke have been documented in some genetic disorders.

Prognosis and complications

The outcome after acute hemiplegia is highly variable and depends on the underlying cause. Data from a large registry of children with arterial ischemic stroke indicate that 54% were neurologically normal, 22% had mild deficits, 17% had moderate deficits, and 8% had severe deficits (33). Among the children with deficits, approximately 60% experienced motor impairments, 30% had difficulties with language, and about 35% exhibited cognitive or behavioral challenges. Acute involvement of the descending corticospinal tract on diffusion-weighted imaging and increasing age at stroke is a harbinger of poor motor outcome (29; 87). Epilepsy develops in 30% of children with arterial ischemic stroke (80). Following intracerebral hemorrhage, 42% of children are normal and 32% have persistent deficits, with 25% mortality, and epilepsy in 11% (61). Alternating hemiplegia of childhood causes mild to severe cognitive problems. Almost all affected children have some level of developmental delay and intellectual disability (94). The prognosis of intracranial infections and acute demyelinating disorders is excellent if diagnosed and treated early. Most patients with reversible cerebral vasoconstriction syndrome show resolution of symptoms within days to weeks. Fifteen to twenty percent are left with residual deficits from stroke (54). The prognosis in posterior reversible encephalopathy syndrome is usually excellent. Symptoms are most often fully reversible after removal of the inciting factor and control of the blood pressure. Serious neurologic disability and death have also been reported (84). Rarely, some patients develop epilepsy after recovery. The outcome of hemiconvulsion-hemiplegia-epilepsy syndrome depends on the cause and immediate seizure control. Most patients develop epilepsy and attacks of status epilepticus. Cognitive deficits are the rule (06). Hemiplegic migraine may recur but does not lead to permanent neurologic deficits in most cases (11). Todd paralysis resolves completely, typically within minutes to hours, though rarely may persist for up to 24 to 48 hours. Functional neurologic disorder has favorable prognosis with appropriate psychological intervention, though some patients experience chronic or recurrent symptoms (105).

Clinical vignette

A 9-year-old girl presented with sudden onset right-sided weakness. She was previously healthy and had no history of recent trauma, infection, or vaccination. There was no family history of premature stroke, myocardial infarction, or deep venous thrombosis. The patient was afebrile and vital signs were normal. Blood pressure was 90/60 mmHg. On neurologic examination, she was fully conscious and cooperative. Cranial nerve examination revealed left central facial paralysis. Strength in the right upper and lower extremities was normal (5/5) but greatly diminished on the left (1/5). Deep tendon reflexes were hyperactive on the left and the left plantar response was extensor. Skin examination revealed no café-au-lait spots, neurofibromas, or freckling of the groin or the axilla. The remainder of the physical examination was normal. Diffusion-weighted magnetic resonance imaging revealed diffusion restriction in the right putamen, nucleus caudatus, and posterior limb of the internal capsule consistent with acute infarction. Time of flight magnetic resonance angiography showed beading and a decrease in caliber in the right supraclinoid segment of the carotid artery and middle cerebral artery. In the superior-anterior part of the M1 segment of the middle cerebral artery, there seemed to be a second lumen with a signal intensity lower than that of the primary lumen but higher than that of the parenchyma. These findings suggested dissection superimposed on fibromuscular dysplasia in the middle cerebral artery, which compromised the origin of the lenticulostriate arteries and led to striatocapsular infarct. Digital subtraction angiography performed 1 week after the MRA showed the typical “string of beads” appearance of fibromuscular dysplasia in the right supraclinoid segment of the carotid artery, M1 and M2 segment of middle cerebral artery, and A1 segment of anterior cerebral artery. Dissection, however, was not confirmed. It was assumed that the dissected intima had sealed during the interval between the MRA and the digital subtraction angiography or that the second lumen appearance resulted from motion artifacts. Abdominal magnetic resonance imaging of the patient was normal. Complete blood count, coagulation parameters, antiphospholipid antibodies, antithrombin III, protein C, protein S, and homocysteine were normal. Factor V Leiden, methylene tetrahydrofolate reductase, and prothrombin G20210A mutations were negative. Serum cholesterol, triglycerides and low- and high-density lipoproteins (LDL, HDL) were 303 mg/dl (122-209), 122 mg/dl (35-114), 221 mg/dl (60-150), and 58 mg/dl (35-84), respectively. Cardiac examinations, including echocardiography and electrocardiography, were normal. The lipid profile of both parents also showed increased levels of cholesterol, triglycerides, and LDL. Familial combined hyperlipidemia was suggested, and a low-cholesterol, low-saturated fat diet was started. Aspirin at a dosage of 3 mg/kg/day was started for its antiplatelet effect and physical rehabilitation was instituted for hemiparesis. No further strokes appeared in the follow-up period of 6 months, and at present, she has mild hemiparesis and is able to walk independently.

Biological basis

Anatomic localization

Acute hemiplegia localizes to lesions affecting the corticospinal tract at any point along its course from the motor cortex through the spinal cord.

The corticospinal tracts arise from somatotopically organized areas of primary motor cortex (Brodmann area 4) in the precentral gyrus, lateral premotor cortex, and supplementary motor area as well as the primary sensory cortex in the postcentral gyrus, ie, the anterior paracentral gyrus, superior parietal lobule, and areas of the cingulate gyrus. The corticospinal tract descends sequentially through (1) the corona radiata; (2) the posterior limb of the internal capsule; (3) the middle three fifths of the cerebral peduncle; (4) the ventral pons, where fibers are dispersed among pontine nuclei and transverse pontocerebellar fibers; (5) the medullary pyramids; (6) the pyramidal decussation at the cervicomedullary junction, where approximately 85% to 90% of fibers cross to form the lateral corticospinal tract whereas 10% to 15% continue ipsilaterally as the anterior corticospinal tract. Thus, lesions in any of these areas can result in hemiparesis of varying degree and distribution.

Corticospinal neurons within the motor cortex are somatotopically organized according to functional importance; the size of the cortical representation in the motor homunculus varies with the functional importance of the body part represented. For example, isolated hand weakness of cortical origin may present with loss of thumb and finger movements and impaired hand flexion and extension, or with only partial involvement of a few digits. The corticospinal tract is also organized somatotopically. In the corona radiata, fibers are widely dispersed. In the posterior limb of the internal capsule, the organization is compact: face and tongue fibers anteriorly, arm fibers centrally, and leg fibers posteriorly. In the cerebral peduncle, face fibers are medial, arm fibers intermediate, and leg fibers lateral. In the pons, fibers controlling proximal muscles lie dorsal to those controlling distal muscles. In the medullary pyramid, leg fibers are lateral to arm fibers and decussate more rostrally.

Lesions restricted to the primary motor cortex produce contralateral weakness respecting somatotopic organization. Small cortical strokes may produce isolated weakness of specific body parts (eg, hand monoparesis from lesions in the hand region, facial weakness from inferior frontal lesions, or leg weakness from superior frontal/paracentral lesions). Large cortical strokes involving the middle cerebral artery territory typically produce face and arm predominant hemiparesis, whereas anterior cerebral artery strokes produce leg predominant weakness. Cortical lesions are typically accompanied by cortical signs, including sensory deficits, visual field deficits, aphasia (if dominant hemisphere), neglect (if nondominant hemisphere), and seizures.

The posterior limb of the internal capsule is a common site for pediatric stroke. Small lesions here can produce pure motor hemiparesis affecting the face, arm, and leg relatively equally due to the compact organization of the motor fibers. Larger lesions may demonstrate face-arm predominant weakness if involving the anterior portion, or leg predominant weakness if involving the posterior portion. Because sensory fibers traverse the posterior portion of the posterior limb, combined motor and sensory deficits can be seen with larger lesions.

Lesions of the basal ganglia, particularly the lentiform nucleus and caudate, can produce contralateral hemiparesis through disruption of motor circuits or involvement of adjacent internal capsule fibers. Associated features may include dystonia, chorea, or other movement disorders.

Lesions in the cerebral peduncle produce contralateral hemiparesis, often accompanied by ipsilateral third nerve palsy (Weber syndrome) if the lesion extends ventrally (85). Pure motor hemiparesis without cranial nerve involvement can occur with small lesions confined to the cerebral peduncle.

Pontine lesions produce several distinctive syndromes. Pure motor hemiparesis with equal involvement of the face, arm, and leg results from small lesions in the basis pontis affecting the corticospinal and corticobulbar tracts. Crossed syndromes (ipsilateral cranial nerve palsies with contralateral hemiparesis) occur with lesions affecting both the corticospinal tract and cranial nerve nuclei or fascicles. Ataxic hemiparesis results from lesions affecting both the corticospinal tract and adjacent pontocerebellar fibers.

Medullary lesions produce contralateral hemiparesis. Associated cranial nerve findings (hypoglossal, vagal, or glossopharyngeal) help distinguish medullary from higher brainstem lesions.

Cervical spinal cord lesions produce ipsilateral hemiparesis because the corticospinal tract has already decussated at the medullary-cervical junction. Brown-Séquard syndrome results from hemisection, causing ipsilateral motor weakness and proprioceptive loss with contralateral pain and temperature sensory loss.

Pathophysiology

Acute hemiplegia in childhood is caused by an alteration in cerebral metabolism in a brain region involved in contralateral motor function. The specific mechanism of this metabolic derangement varies depending on the underlying cause.

Stroke. The pathogenesis of childhood stroke is multifactorial, and stroke in children differs substantially from adult stroke in both etiology and vascular biology. The most common cause of childhood stroke is arteriopathy (38). These include arterial dissection and focal cerebral arteriopathy of childhood (FCA) (104). FCA is increasingly recognized as an immune-mediated, often postinfectious arteriopathy characterized by transient or progressive focal narrowing of large intracranial arteries, most commonly the distal internal carotid artery or proximal middle cerebral artery. Localized vessel inflammation promotes endothelial dysfunction, platelet activation, and secondary thrombus formation. Arterial dissection, affecting either extracranial or intracranial vessels, results from disruption of the arterial intima, leading to intramural hematoma, luminal narrowing, and embolization. Trauma is a frequent precipitating factor in dissections. Moyamoya disease is a progressive occlusive arteriopathy involving the distal internal carotid arteries and their proximal branches, leading to chronic cerebral hypoperfusion and development of fragile collateral networks. Moyamoya disease is associated with 6% to 10% of childhood strokes and transient ischemic attacks. Genetic susceptibility, particularly involving RNF213 variants, plays an important role. Ischemic stroke and transient ischemic attacks predominate in children, whereas hemorrhage is more common in adults. Cardioembolic stroke occurs as a result of congenital heart disease, acquired heart disease, and procedure-related events. The pathophysiology of stroke in children with cardiac disease is usually thromboembolic, and abnormal intracardiac flow, endothelial injury, and hypercoagulability contribute to embolus formation. Thrombophilia leads to hypercoagulable states resulting from inherited or acquired conditions. Prothrombotic conditions may act as triggers for stroke in the presence of other risk factors. Systemic causes of childhood stroke include inflammatory causes and genetic/metabolic syndromes. Typical examples include primary angiitis of the central nervous system, systemic lupus erythematosus, and polyarteritis nodosa. Clues for inflammatory causes include proteinuria, presence of persistent serum inflammatory markers, frequent fevers, and livedo reticularis. Genetic and metabolic causes of stroke are rare. ACTA2 syndrome, COL4A1 mutations, and PHACE syndrome are specific syndromes. Stroke in mitochondrial disorders does not follow typical arterial distributions (35). Risk factors and causes of pediatric arterial ischemic stroke are shown in Table 1.

Table 1. Risk Factors for and Causes of Pediatric Arterial Ischemic Stroke

	Cardiac	Congenital Complex congenital heart diseases (cyanotic> acyanotic) Patent foramen ovale Acquired Arrhythmia ECMO Endocarditis Myocarditis Prosthetic heart valve Rheumatic heart disease
	Arteriopathy	Inflammatory/parainfectious External dissection Focal cerebral arteriopathy Post-varicella and other viral angiopathies Primary CNS vasculitis of childhood Transient cerebral arteriopathy Infectious Meningitis (viral, bacterial, tuberculosis) Dissection Moyamoya disease (idiopathic) Spontaneous/traumatic Moyamoya syndrome Down syndrome Neurofibromatosis type 1 Systemic vasculitis/secondary CNS vasculitis Adenosine deaminase-2 deficiency Behcet disease Inflammatory bowel disease Kawasaki disease Polyarteritis nodosa Systemic lupus erythematosus Takayasu arteritis Post-radiation vasculopathy Reversible segmental cerebral vasoconstriction Migraine Connective tissue diseases Ehlers-Danlos syndrome Marfan syndrome Genetic vasculopathies PHACES, ACTA2 mutation, Alagille syndrome Dynamic vertebral artery compression/V3 pseudoaneurysm
	Hematologic	Acquired thrombophilias Inherited thrombophilias Leukemia/lymphoma Nephrotic syndrome Sickle cell anemia Thalassemias
	Drugs	Chemotherapy (L-asparaginase) Cocaine, methamphetamine, ecstasy, ergot alkaloids, triptans Oral contraceptives
	Metabolic	Homocystinuria Fabry disease

Intracranial hemorrhage. Hemorrhage causes hemiplegia as a result of mass effect or disruption of corticospinal tracts. Hemorrhages can be caused by vascular malformations (about 50%), brain tumors (10%), cardiac disease, hematological disorders, and medical illnesses (25%) (60; 92). In some cases, there is no identifiable cause. Intraparenchymal hemorrhages are generally due to vascular malformations or brain tumors (60). Subdural hemorrhages generally occur in the setting of hematological disorders or cardiac surgery. Subarachnoid hemorrhage is not associated with specific risk factors (60).

Metabolic or genetic disorders. Metabolic abnormalities, such as hyper- and hypoglycemia and electrolyte abnormalities, impair neuronal energy supply and synaptic transmission, leading to focal neurologic deficits. Inherited metabolic disorders can cause stroke-like episodes with hemiplegia, which are mediated by cellular energy failure, for example, in mitochondrial disorders like MELAS and organic acidemias. Genetic disorders may also predispose to cerebrovascular disease through abnormalities of vascular integrity, smooth muscle function, or extracellular matrix composition (72; 51).

Hemiplegic migraine. Migraine auras of all types are due to cortical spreading depression characterized by brief neuronal excitation, which initiates a depolarization wave that moves across the cortex at a rate of 3 to 5 mm/minute and is followed by prolonged inhibition of neuronal activity (82). Whether hemiplegic migraine is qualitatively different from other migraines with aura is debatable. Mutations affecting ion channels and neuronal excitability, including calcium channels, sodium channels, and sodium-potassium ATPase function (CACNA1A, SCN1A, and ATP1A2), account for a substantial proportion of familial cases and are inherited in an autosomal dominant pattern (22).

Seizures: Todd paralysis and ictal hemiplegia. “Neuronal exhaustion” is considered the most likely cause of Todd paralysis. Todd believed in the context of his electrical theory of epilepsy that the hemiparesis resulted from undue exultation resulting in a state of depression or exhaustion (30). Excessive inhibition is another proposed mechanism. Epileptic activity in the supplementary motor area or somatosensory cortex (20) or temporoinsular area (101) has been implicated in epileptic hemiparesis. Periodic lateralizing epileptiform discharges on EEG may be disproportionately frequent during ictal hemiparesis. Although the pathophysiological mechanism of hemiconvulsion-hemiplegia-epilepsy syndrome is not known, there are several factors that are believed to contribute to the pathogenesis. Proposed mechanisms include seizure-induced cytotoxic edema, inflammatory cytokine damage, and prolonged ictal activity (95).

Demyelinating disorders. Demyelination in the cerebral white matter or the spinal cord results in hemiplegia primarily by slowing conduction through motor fibers.

Infection. Meningitis and encephalitis can cause hemiplegia via the destruction of brain parenchyma, abscess formation, local inflammation, or infection-related vasculopathy (16). Both ischemic and hemorrhagic mechanisms may be involved, depending on the pathogen and host immune response.

Neoplasm. A tumor may cause hemiplegia through compression of brain or cervical cord structures responsible for motor control by the mass lesion itself or surrounding edema or hemorrhage.

Head or neck trauma. Head trauma can cause acute hemiplegia through a variety of mechanisms, including shearing injury; intraparenchymal, epidural, subdural, or subarachnoid hemorrhage; or ischemic injury, which can be a primary effect due to dissection or secondary to vasospasm following subarachnoid hemorrhage. Repeated head trauma, as occurs in the setting of contact sports, may increase the risk of brain ischemia over time due to long-term vascular and neuronal changes (13). Acute cervical cord compression causing hemiplegia may be spontaneous or the result of trauma (37).

Toxin or medication side effects. Toxic agents produce stroke via a range of mechanisms like vasculopathy (eg, cocaine) or cause hemiplegia through myelin and axon loss, gliosis, and necrosis (eg, methotrexate leukoencephalopathy) (57).

Functional neurologic disorders. Functional neurologic disorder presents with hemiplegia in the absence of structural or metabolic brain disease. Atypical activation in the motor cortex, basal ganglia, and thalamus in response to paretic limb stimulation (59) and atypical connectivity between the amygdala and the supplementary motor area (102) as well as between the ventromedial and dorsolateral prefrontal cortex (23) are present in patients with functional neurologic disorder. Motor mental imagery is impaired (14). Together these data suggest an atypical relationship between emotion and motor function (102).

Posterior reversible encephalopathy syndrome. The pathophysiology involves failure of cerebrovascular autoregulation leading to vasogenic edema, though cytotoxic edema may coexist and indicates more severe injury. When hypertension exceeds cerebrovascular autoregulatory limits, it results in endothelial dysfunction and failure of compensatory vasoconstriction to prevent hyperperfusion and subsequent fluid extravasation. Because sympathetic innervation is relatively scant in the posterior circulation, parieto-occipital lobes are affected frequently. Antineoplastic and immunosuppressive drugs may also cause a direct toxic effect on the cerebrovascular endothelium (39).

Reversible cerebral vasoconstriction syndrome. The pathophysiology of the abrupt-onset headache and the prolonged-reversible vasoconstriction in RCVS is not known. Transient dysregulation of the cerebrovascular tone is suggested. Cerebral vasoconstriction may result in ischemic stroke or hemorrhages in some cases (99).

Alternating hemiplegia of childhood. About 80% of cases are caused by mutations in the ATP1A3 gene, which encodes the alpha3 subunit of Na+/K+-ATPase. This pump is critical for maintaining ion gradients across neuronal cell membranes and regulating neuronal excitability (83). ATP1A3 is highly expressed in neurons, particularly in the basal ganglia, brainstem, and cerebellum. Mutations impair the pump's function, disrupting ion homeostasis and leading to aberrant neuronal firing patterns, leading to recurrent, reversible hemiplegic episodes often triggered by stress or exertion. Alternating hemiplegia is fundamentally a channelopathy (67).

Differential diagnosis

Confusing conditions

The differential diagnosis of acute hemiplegia is extremely broad, although stroke, migraine, and Todd paralysis are the most common causes (Table 2).

Table 2. Differential Diagnosis of Acute Hemiplegia in Children

Condition	History	Clinical features	Investigations
Acute disseminated encephalomyelitis	Preceding viral illness or vaccination (1–2 weeks), subacute onset, altered state of consciousness	Encephalopathy, multifocal neurologic deficits, optic neuritis, may have spinal cord involvement	MRI: multifocal, asymmetric T2/FLAIR hyperintense lesions (white matter + deep gray), large, poorly demarcated CSF: lymphocytic pleocytosis, elevated protein, oligoclonal bands often absent
Alternating hemiplegia	Developmental delay, abnormal eye movements, onset before 18 months, recurrent episodes, family history rare, progressive cognitive impairment	Binocular or monocular nystagmus, hemiplegic and dystonic attacks shifting from side to side, complete resolution with sleep, recurrence on awakening, episodes last minutes to days	Genetic testing: ATP1A3 (85%) MRI: typically normal or nonspecific EEG: normal or nonspecific slowing during attacks Echocardiography/ECG: arrhythmias, cardiomyopathy
Arterial ischemic stroke	Sudden onset Risk factors: cardiac disease, sickle cell disease, arteriopathy, recent infection, neck trauma, prothrombotic disorder	Acute focal deficit, inability to walk, hemiparesis, speech problems, facial paralysis, may have seizures	MRI/DWI: restricted diffusion in arterial territory MRA: vessel occlusion/stenosis Echocardiography, thrombophilia panel, hemoglobin electrophoresis
Cerebral sinovenous thrombosis	Risk factors: dehydration, infection (mastoiditis, sinusitis), prothrombotic state, L-asparaginase therapy, inflammatory bowel disease, nephrotic syndrome	Headache, vomiting, papilledema, seizures common, bilateral or unilateral deficits, may have hemorrhagic venous infarction	MRI/MRV: filling defect in dural sinus CT: "empty delta sign," venous infarction (hemorrhagic or non-hemorrhagic), thrombophilia screening
Cervical cord compression	Neck trauma, atlantoaxial instability, tumor, epidural abscess	Ipsilateral hemiparesis (below lesion level), sensory deficits, bowel/bladder dysfunction, may have respiratory compromise if C4 or above	Urgent spine MRI: cord compression, signal abnormality
CNS infections (meningitis/encephalitis)	Fever, headache preceding respiratory/gastrointestinal illness, immunocompromised state	Signs of meningeal irritation, fever, altered consciousness, seizures, focal deficit, rash (meningococcemia)	MRI: meningeal enhancement, parenchymal signal abnormality, vasculitis, abscess CSF: pleocytosis, elevated protein, ± low glucose, viral PCR, cultures, tuberculosis studies
CNS tumor	Progressive symptoms over days to weeks, morning headache/with Valsalva, vomiting, may have acute worsening (hemorrhage, hydrocephalus)	Progressive or stuttering deficit, cranial nerve palsies, ataxia, papilledema	MRI with contrast: mass lesion with enhancement, mass effect, edema, may have hemorrhage Biopsy: tissue diagnosis
Functional neurologic disorder	Disproportionate effect on function, psychological stressors	Findings not conforming to a neuroanatomical condition, inconsistent weakness (varies with attention/distraction), symptoms improve with suggestion/distraction, Hoover sign positive	Normal investigations, diagnosis of exclusion
Hemiplegic migraine	Recurrent headache, family history, complete resolution between attacks	Hemiparesis with typical auras (visual > somatosensory > dysphasic), headache typically follows or accompanies aura, episodes last hours to days, complete recovery	MRI: normal or transient perfusion changes (hypoperfusion or hyperperfusion) Genetic testing
Intracranial hemorrhage	Abrupt onset, signs of increased intracranial pressure, severe headache ("worst headache"), vomiting, declining consciousness Risk factors: AVM, aneurysm, coagulopathy, tumor, trauma	Rapid evolution of neurologic findings, sudden severe headache, vomiting, coma, focal deficit, meningismus if SAH component	CT: hyperdensity (acute blood) CTA/MRA: vascular malformation, aneurysm Coagulation studies
Mitochondrial disorders	Hypotonia, developmental regression, vomiting, encephalopathy, consanguinity, short stature, hearing loss, diabetes	Stroke-like episodes, seizures, lactic acidosis during acute episodes, progressive encephalopathy	MRI: lesions not following vascular distribution Lactate peak on MRS, genetic, elevated serum/CSF lactate, muscle biopsy
Posterior reversible encephalopathy syndrome	Seizures, headache, acute hypertension (may be normotensive) Predisposing: renal disease, immunosuppression, chemotherapy, autoimmune disease	Hypertension, seizures, altered state of consciousness, visual disturbance	MRI: symmetric posterior-predominant vasogenic edema (T2/FLAIR hyperintense, usually no restricted diffusion)
Postictal (Todd) paralysis	Focal motor seizure, history of epilepsy	Hemiparesis following seizure, gradual resolution over minutes to hours (typically < 24 hours, most < 48 hours)	EEG: postictal slowing MRI: normal or transient peri-ictal abnormalities (restricted diffusion in cortex), resolves completely
Reversible cerebral vasoconstriction	Thunderclap headache, history of vasoactive drugs	Severe thunderclap headache, may have seizures, altered state of consciousness, focal neurologic findings	MRI: may show ischemic or hemorrhagic stroke MRA: "string-of-beads" VWI: no vessel wall enhancement

In the differential diagnosis of hemiplegia in children, the clinician should first distinguish between peripheral and central deficits. A detailed history, including perinatal events, family history, and recent infections, alongside a competent neurologic examination and targeted neuroimaging with vascular studies is essential for accurate diagnosis. Upper motor neuron facial weakness, encephalopathy, and seizures should point the clinician to central nervous system. Increased tone and reflexes on the affected side are late signs of hemiplegia due to central deficits. The signs in younger children are more diffuse and the clinician should be careful with asymmetry of movements, tone, posture, and reflexes. The immediate priority in the acute setting is to identify a neurosurgical emergency such as intracranial hemorrhage, malignant ischemic stroke, brain tumor, and hydrocephalus. An abrupt onset with headache and coma is suggestive of intracranial hemorrhage. Headache is common in hemiplegic migraine, central nervous system infections, and sinovenous thrombosis. Cases with hemiplegic migraine also have more typical auras (visual, sensory, or dysphasic) often cooccurring with the hemiplegia. Encephalopathy is common in central nervous system infections and acute demyelinating disorders. Thunderclap headache is common in cerebral vasoconstriction syndrome and subarachnoid hemorrhage. Children with moyamoya disease have transient ischemic attacks that are triggered by hyperventilation, dehydration, or crying. During attacks of alternating hemiplegia, paralysis alternates from one side of the body to the other. Symptoms completely disappear with sleep and reappear with awakening. Seizures are often the presenting manifestation associated with visual disturbances in posterior reversible encephalopathy syndrome (09).

Diagnostic workup

A focused history should include time of onset, mode of progression, precipitating factors, prior similar episodes, recent infection, trauma, drug exposure, and systemic illness. Family history is relevant in suspected genetic conditions, such as hemiplegic migraine, alternating hemiplegia of childhood, connective tissue disorders, and thrombophilia syndromes. Clinical examination provides crucial clues about the cause of hemiplegia. Fundoscopic examination may reveal signs of retinal hemorrhage, suggesting trauma, as well as signs of a genetic disorder like Lisch nodules or cataracts. Examination of the oropharynx and neck may reveal evidence of injury or inflammation. Examination of the heart facilitates the diagnosis of cardiac disease. Delayed or diminished femoral pulses suggest coarctation of the aorta, which has been associated with Moyamoya disease. Examination of the skin may reveal lesions of varicella or herpes infection, abnormalities of Ehlers-Danlos syndrome or other connective tissue disorder, stigmata of neurocutaneous disorders, or lesions of conjunctivae and skin, suggesting Kawasaki or Behçet disease.

Neuroimaging. Neuroimaging is essential in the evaluation of a child with acute hemiplegia. Computed tomography (CT) is rapid and appropriate for emergent evaluation, particularly to exclude hemorrhage, but it is inadequate, except for perfusion-weighted imaging, to detect early ischemic stroke and may miss stroke mimics (86; 01; 88). Magnetic resonance imaging (MRI) with diffusion-weighted imaging sequences with apparent diffusion coefficient maps is the most sensitive test for arterial ischemic stroke (03). Diffusion- and perfusion-weighted imaging can detect ischemia within minutes. Abnormalities on T2-weighted and FLAIR imaging usually become visible after approximately 4.5 hours. Gradient echo imaging detects blood.

Magnetic resonance angiography (MRA) is probably equivalent to standard angiography for carotid and middle cerebral artery angiopathies, but it is less sensitive for small vessel disease and distal angiopathy (12). In some cases, cerebral angiography may be required to better delineate suspected arterial dissection, moyamoya disease, fibromuscular dysplasia, or vasculitis (81). MRA can overestimate the length and severity of stenosis. MRA can also identify aneurysms larger than 3 mm. A 3D CT angiography may have value in the evaluation of arterial ischemic stroke and arteriopathies, but the amount of radiation is relatively high, and its utility in pediatric cases is not well studied (79). Abnormal cerebral angiography is the primary diagnostic feature of reversible vasoconstriction syndrome. Smooth, tapered narrowing followed by dilated segments of second and third order cerebral arteries, resulting in a “sausage on a string” appearance, is the most characteristic abnormality.

MRI can also provide some information about the presence of vasculopathies. High-resolution, fat-saturated, T1-weighted vessel wall imaging with and without contrast should be performed to evaluate for arterial dissection or other vasculopathy (28). Vessel wall imaging provides additional insights beyond traditional angiographic studies that only assess the arterial lumen. Patterns of wall thickening and enhancement may help distinguish inflammatory arteriopathies from noninflammatory vasculopathies. In particular, vessel wall imaging helps differentiate arterial dissection from inflammatory arteriopathies. Moyamoya disease can be diagnosed on MRI based on its dilated, tortuous enhancing signal voids in the basal ganglia and the severe stenosis of the distal internal carotid artery (07).

In hemorrhagic stroke, CT may identify acute bleeding but may not identify underlying vascular abnormalities, such as arteriovenous malformations and cavernomas, and it may poorly differentiate tumors from secondary hemorrhage. Therefore, an MRI with and without contrast enhancement and MRA should be obtained. Susceptibility-weighted brain MRI can identify small cavernous malformations or tumors, whereas angiography offers greater resolution for detecting arteriovenous malformations, arteriovenous fistulas, and aneurysms (93).

Specific patterns on MRI may aid in defining etiology, especially in mitochondrial disorders. Stroke-like lesions that do not conform to vascular territories, which are bilateral, and the presence/absence of basal ganglia signal abnormalities may be clues to an underlying mitochondrial disorder. Subsequent MR spectroscopy is useful to aid in identifying certain mitochondrial disorders by evaluating for lactate peaks in noninfarcted areas (58).

Typical findings of PRES are bilateral areas of white matter edema in the posterior cerebral hemispheres, but variations do occur. Demyelinating disorders, including MOG antibody-associated disease, often demonstrate multifocal white matter lesions not confined to vascular territories.

Tumor, demyelination, leukoencephalopathy, and evidence of trauma are best detected using MRI. Transient abnormalities have been described on MRI with both hemiplegic migraine and prolonged focal seizures (98).

Laboratory investigations. Initial laboratory testing should include complete blood count, inflammatory markers, coagulation studies, and serum chemistries. These may identify infection, hematologic disease, or metabolic disturbances. Blood cultures are necessary for diagnosing bacterial endocarditis. Urine drug screen for cocaine and amphetamines may identify a toxicological cause of stroke. Routine urinalysis provides information about possible renal disease and dehydration. Cardiac evaluation includes electrocardiography, echocardiography (transthoracic and transesophageal when indicated), and prolonged cardiac monitoring to identify arrhythmias, structural heart disease, or intracardiac thrombi when embolic stroke is suspected. Lumbar puncture is performed when central nervous system infection or inflammatory disease is suspected. Thrombophilia testing should include factor V Leiden, prothrombin G20210A mutation, protein C and S deficiency, antithrombin deficiency, antiphospholipid antibodies, homocysteine, and lipoprotein(a). Acute phase reactants may affect protein C, protein S, and antithrombin levels; repeat testing after acute illness may be necessary (35). Metabolic investigations may include serum and cerebrospinal fluid lactate, plasma amino acids, acylcarnitine profile, and urine organic acids. These studies are particularly informative during acute metabolic decompensation. Genetic testing for common mitochondrial mutations and measurement of respiratory chain activities in muscle is required to establish the diagnosis of mitochondrial encephalomyopathies (09).

Genetic testing is indicated in suspected hemiplegic migraine, alternating hemiplegia of childhood, mitochondrial disorders, and other inherited vasculopathies. The genetic landscape of hemiplegic migraine continues to expand. Although mutations in CACNA1A (FHM1), ATP1A2 (FHM2), and SCN1A (FHM3) account for approximately 25% of cases, approximately 75% of patients with hemiplegic migraine remain genetically unexplained.

Prevention

Risk factors for stroke in children differ significantly from those in adults. Widespread vaccination against Haemophilus influenzae and Streptococcus pneumoniae has decreased the incidence of bacterial meningitis and its complications, including stroke. Similarly, vaccination against varicella may have decreased the frequency of post-varicella focal cerebral arteriopathy. In sickle cell disease, transcranial Doppler screening and chronic transfusion therapy significantly reduce stroke risk and recurrence (21). It is important to establish healthy behaviors in childhood to reduce the risk of obesity and sedentary lifestyle (35). Children with metabolic and genetic disorders underlying stroke may benefit from treatment of their underlying condition. Medication management to prevent migraine and seizures presumably decreases the frequency of hemiplegic migraine and Todd paralysis.

Management

Management depends on the cause of hemiplegia and differs significantly among stroke, hemorrhage, epilepsy, migraine, and infection as well as demyelinating, metabolic and genetic disease.

Stroke. Several consensus guidelines and algorithms for the management of different types of strokes have been published (71; 35; 68; 92). The 2026 American Heart Association/American Stroke Association Guideline for the Early Management of Patients with Acute Ischemic Stroke represents the first comprehensive guidance on pediatric stroke, including specific recommendations on intravenous alteplase within 4.5 hours of symptom onset and mechanical thrombectomy for selected children with large-vessel occlusion (78). However, these recommendations are largely extrapolated from adult data and observational pediatric series. Treatment decisions should be made with neurologists and endovascular surgeons with experience in treating children (35; 91).

Treatment of hypertension, hypotension, fever, hyperglycemia, and seizures is essential. Decompressive hemicraniectomy should be considered for large strokes associated with mass effect and deterioration of consciousness (90). Antithrombotic therapy recommendations are based on stroke etiology. Early anticoagulation is reasonable pending etiologic evaluation, given the relatively high likelihood of arterial dissection, cardiac disease, or hypercoagulable states in children (35). Once high-risk etiologies are ruled out, anticoagulation can be stopped and aspirin substituted for secondary stroke prevention. The duration of aspirin therapy depends on the underlying condition. Most children are treated for 2 years to cover the time window when the vast majority of recurrent strokes occur (71). If arterial ischemic stroke is due to cardiac embolism, extracranial arterial dissection, or hypercoagulable state, long-term anticoagulation is recommended. In sickle cell disease, acute exchange transfusion followed by long-term transfusion therapy is standard care (21). Revascularization surgery is recommended for Moyamoya disease if symptoms of ischemia increase or if cerebral perfusion is compromised (05). With strokes due to cerebral venous sinus thrombosis, the precipitating illness and seizures and elevated intracranial pressure, if present, require treatment. Anticoagulation both acutely and chronically is recommended (3 to 6 months) (35), particularly given the fact that thrombus propagation may occur in over one third of untreated children (70). Treatment of stroke due to genetic and metabolic conditions varies by disorder.

Traditional rehabilitation is appropriate for hemiplegia of any cause. Techniques, such as constraint-induced movement therapy and transcranial magnetic stimulation, have shown potential in improving motor skills by promoting neuroplasticity in the developing brain (42; 49).

Hemorrhagic stroke. In the acute setting, children with cerebral hemorrhage should be stabilized medically. Acute stabilization includes blood pressure management, reversal of coagulopathy if present, and management of elevated intracranial pressure (35). Surgical or endovascular intervention may be indicated for accessible large hematomas causing mass effect, posterior fossa hemorrhages with hydrocephalus or brainstem compression, and vascular lesions, such as arteriovenous malformations, aneurysms, or arteriovenous fistulas amenable to treatment (08).

Seizures. Appropriate EEG monitoring and choice of antiepileptic medication therapy is crucial to seizure control.

Alternating hemiplegia of childhood. Flunarizine, a calcium channel blocker, has been shown to reduce the duration, severity, and frequency of episodes of alternating hemiplegia, but has no abortive effects (83). Flunarizine is not currently approved by the U.S. FDA or its counterpart in Japan. Theoretically, flunarizine works by modulating dysfunctional calcium and sodium-potassium ATPase channels related to ATP1A3 mutations. However, flunarizine has not been shown to have a significant effect on the overall developmental outcome. Various treatments have been tried with differing levels of success in aborting attacks or reducing the frequency and severity of paroxysmal episodes. These include benzodiazepines, flunarizine, topiramate, the ketogenic diet, triheptanoin, steroids, amantadine, memantine, aripiprazole, oral ATP, coenzyme Q, acetazolamide, dextromethorphan, and vagus nerve stimulation (83).

Hemiplegic migraine. Flunarizine, valproate, and steroids have been used to treat prolonged auras acutely (103). Intranasal ketamine has been used to treat hemiplegic aura (55). Calcium channel blockers and valproate are the most commonly used preventative agents in hemiplegic migraine (103; 76). Beta blockers and triptans should be avoided (56; 46).

Demyelinating disorders. Acute disseminated encephalomyelitis generally responds to treatment with corticosteroids or intravenous immunoglobulins (19). Plasma exchange is suggested in cases who fail to respond to steroids and intravenous immunoglobulins.

Functional neurologic disorder. Multidisciplinary treatment is essential (100). Physical therapy with a positive, nonconfrontational approach focuses on restoring normal movement patterns. Cognitive behavioral therapy addresses underlying psychological stressors, and pharmacotherapy targets comorbid depression or anxiety.

Reversible cerebral vasoconstriction syndrome. There is no established therapy for RCVS. Most patients fully recover with supportive care, including hospitalization for monitoring, pain control with analgesics, and avoidance of precipitating factors (sympathomimetics, vasoactive substances). Calcium channel blockers, such as nimodipine and verapamil, serotonin antagonists, dantrolene, and brief courses of magnesium sulfate, have been helpful in some studies (31).

Posterior reversible encephalopathy syndrome. PRES should be promptly recognized because it is usually reversible with appropriate treatment. Gradual blood pressure lowering will often improve the patients dramatically. Overaggressive blood pressure lowering can lead to complications. Seizures are treated with antiseizure drugs. Reduction of drug dose or prompt removal of the cytotoxic or immunosuppressive drug is recommended (36).

Anesthesia

Specific anesthetic management is required in children who are at high risk for stroke due to moyamoya (avoiding hyperventilation, maintaining adequate hydration and blood pressure) (44) or sickle cell disease (avoiding hypoxia, hypothermia, dehydration) (66).

Outcomes

There are no clinical trials evaluating the best treatment for childhood arterial ischemic stroke (anticoagulant or antiplatelet medication). Recurrent stroke risk varies by etiology and antithrombotic management. Overall recurrence rates are approximately 6% to 19% within 5 years (25). It is well known that the absence of antithrombotic therapy increases the risk of recurrent stroke by 1.5- to 2-fold. The use of anticoagulation is relatively safe in children with arterial ischemic stroke, with a 4% risk of intracerebral hemorrhage. Safety and efficacy data for hyperacute stroke therapies in children are lacking. Decompressive craniotomy results in decreased mortality and improved outcomes in patients with large cerebellar infarctions (35). Functional outcomes after pediatric stroke are highly variable. Approximately 50% to 70% of children have persistent neurologic deficits, though many achieve good functional independence. Younger age at stroke, larger infarct volume, involvement of dominant hemisphere or basal ganglia, and recurrent stroke predict worse outcomes. Hemiparesis is the most common sequela, occurring in 40% to 60% of survivors. Long-term sequelae include epilepsy, cognitive impairment, and behavioral difficulties. Hemiplegic migraine outcomes are generally favorable. Flunarizine is associated with more than 50% reduction in attack frequency in 85% of pediatric hemiplegic migraine (76). Most children experience decreasing attack frequency with age, though some develop chronic migraine. The long-term effect of preventive therapies on disease trajectory is unknown. Alternating hemiplegia of childhood has variable outcomes. Developmental delay and intellectual disability occur in 50% to 80%, often related to cumulative effects of repeated episodes and underlying ATP1A3 dysfunction. Flunarizine improves episode frequency and severity but does not alter long-term developmental prognosis (77). PRES and reversible cerebral vasoconstriction syndrome generally have favorable prognoses with supportive care. Most patients with demyelinating disorder of the central nervous system make a full but slow recovery with steroids over 4 to 6 weeks. Approximately 10% to 20% have residual deficits or develop recurrent demyelination (multiple sclerosis or neuromyelitis optica spectrum disorder).

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Authors

Haluk Topaloglu MD

Dr. Topaloglu of Hacettepe Children's Hospital in Ankara, Turkey, has no relevant financial relationships to disclose.
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Hatice Bektaş MD

Dr. Bektaş of Ankara Bilkent City Hospital has no relevant financial relationships to disclose.
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Nina F Schor MD PhD

Dr. Schor of the University of Rochester School of Medicine and Dentistry has no relevant financial relationships to disclose.
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David A Griesemer MD
Timothy D Carter MD
Sabrina E Smith MD PhD
Lawrence W Brown MD
Belinda Oyinkan Marquis MD
Heather A Lau MD
Ruth Nass MD
Kimon Bekelis MD
Robert J Singer MD
Uluc Yis MD

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Acute hemiplegia in childhood

Differential Diagnosis

Acute disseminated encephalomyelitis
Alternating hemiplegia
Arterial ischemic stroke
Cerebral sinovenous thrombosis
Cervical cord compression
- CNS infections (meningitis/encephalitis)
- CNS tumor
- Functional neurologic disorder
- Hemiplegic migraine
- Intracranial hemorrhage
- Mitochondrial disorders
- Posterior reversible encephalopathy syndrome
- Postictal (Todd) paralysis
- Reversible cerebral vasoconstriction

Also Relevant

Alternating hemiplegia of childhood
Cerebral palsy
Chemotherapy: neurologic complications
Hemiconvulsion-hemiplegia-epilepsy syndrome
Hemiplegic migraine
- Illicit drug use: neurologic complications
- Moyamoya disease
- Porencephaly
- Stroke associated with sickle cell disease
- Stroke in young adults
- Sturge-Weber syndrome

Acute hemiplegia in childhood

Cite this article

Introduction

Overview

Key points

Historical note and terminology

Clinical manifestations

Presentation and course

Prognosis and complications

Clinical vignette

Biological basis

Anatomic localization

Pathophysiology

Table 1. Risk Factors for and Causes of Pediatric Arterial Ischemic Stroke

Epidemiology

Differential diagnosis

Confusing conditions

Table 2. Differential Diagnosis of Acute Hemiplegia in Children

Diagnostic workup

Prevention

Management

Anesthesia

Outcomes

References

Contributors

Authors

Editor

Former Authors

Patient Profile

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