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PubMed2002

Hemiconvulsion-hemiplegia-epilepsy syndrome: characteristic early magnetic resonance imaging findings.

We report three patients with hemiconvulsion-hemiplegia-epilepsy syndrome who presented acutely and were shown to have striking neuroimaging findings suggestive of diffuse cytotoxic edema confined to one hemisphere, including extensive diffusion-weighted imaging abnormalities in two cases. Two patients subsequently developed progressive and extensive atrophy of the involved hemisphere. These findings are consistent with earlier descriptions of the classic neuroradiologic features of this syndrome and are helpful in the differential diagnosis of acute infantile hemiplegia. Further, the findings support the previously proposed pathogenetic mechanism of neuronal injury caused by status epilepticus.

Aspartic Acid↗
PubMed2002

Hemiconvulsion-hemiplegia syndrome and elevated interleukin-6: case report.

We report a 2-year-old boy who developed hemiconvulsion-hemiplegia syndrome with left-sided hemiplegia after a seizure lasting 35 minutes. The interleukin-6 level in the cerebrospinal fluid 2 hours after seizure onset was elevated to levels seen in patients with encephalitis. At 1 year after onset of the seizure, the patient remained hemiplegic on the left side, and magnetic resonance imaging showed severe right hemispheric atrophy. Acute changes seen on imaging studies and electroencephalograms in this patient were consistent with seizure-induced brain damage. Elevation of cerebrospinal fluid interleukin-6 may be related to the severe neurologic sequelae of our patient despite the relatively short seizure duration.

Acute Disease↗
PubMed2002

Association between factor V Leiden mutation and the hemiconvulsion, hemiplegia, and epilepsy syndrome: report of two cases.

The factor V Leiden mutation is the most common hereditary cause of venous thrombosis in our population. In the pediatric population, it has been associated with cerebrovascular thrombosis, cerebral palsy, and prosencephaly in neonates. We present two children with hemiconvulsion, hemiplegia, and epilepsy syndrome in whom the cause is likely attributable to the factor V Leiden mutation. We suggest that patients presenting with hemiconvulsion, hemiplegia, and epilepsy syndrome should be routinely investigated for factor V Leiden, and, if positive, careful consideration should be given to therapeutic and prophylactic anticoagulation as this may improve long-term outcome.

Adolescent↗
PubMed1993

Alternating hemiplegia syndrome: electroencephalogram, brain mapping, and brain perfusion SPECT scan study in a Chinese girl.

A 3-year-old Chinese girl with alternating hemiplegia syndrome failed to respond to anticonvulsants, antimigrainous drugs, and calcium channel blockers. She made a complete remission with a 4-week course of steroid, and relapsed after steroid withdrawal. Electroencephalogram and brain mapping during the hemiplegic attack showed unilateral high-voltage sharp slow-wave discharges in the temporo-occipital region contralateral to the hemiplegic side and diffuse high-voltage slowing during attacks of quadriplegia or other clinical manifestation such as dullness, lethargy, or yawning. Brain perfusion single photon emission computed tomographic (SPECT) scan study during the attack showed decreased uptake in the temporoparietal region contralateral to the hemiplegic side and in the ipsilateral basal ganglia, whereas the perfusion was normal between attacks. Electroencephalogram background activity was improved while the child was in clinical remission with steroid treatment. Computed tomographic and magnetic resonance imaging scans of the brain were normal. Carotid angiogram failed to show any structural or dynamic changes of the carotid arteries. The possible mechanism underlying alternating hemiplegia syndrome might be transient and reversible cerebral ischemia with high-voltage slow-wave discharges shown in the electroencephalogram and decreased perfusion in SPECT scan.

Betamethasone↗
PubMed1998

Alternating hemiplegia of childhood: insights into its pathophysiology.

Alternating hemiplegia of childhood is a rare disorder characterized by episodic paroxysmal attacks of neurologic dysfunction and has historically been thought to represent a migraine equivalent, an unusual form of epilepsy, or a movement disorder. Medical treatment with a variety of anticonvulsants and migraine agents is largely unsuccessful, and progressive mental deterioration is universally expected. Despite extensive laboratory studies, the pathophysiologic basis of this condition has thus far eluded identification. Recently, an international workshop was held to generate testable hypotheses regarding the pathophysiology of alternating hemiplegia of childhood. This paper summarizes the major proceedings of that workshop, and hopes to stimulate further interest in elucidating the molecular and cellular mechanisms underlying this unusual disorder.

Brain↗
PubMed2005

A new method for predicting functional recovery of stroke patients with hemiplegia: logarithmic modelling.

OBJECTIVE: To examine the validity and applicability of logarithmic modelling for predicting functional recovery of stroke patients with hemiplegia. DESIGN: Longitudinal postal survey. SUBJECTS: Stroke patients with hemiplegia staying in a long-term rehabilitation facility, who had been referred from acute medical service 30-60 days after onset. METHODS: Functional Independence Measure (FIM) scores were periodically assessed during hospitalization. For each individual, a logarithmic formula that was scaled by an interval increase in FIM scores during the initial 2-6 weeks was used for predicting functional recovery. RESULTS: For the study, we recruited 18 patients who showed a wide variety of disability levels on admission (FIM scores 25-107). For each patient, the predicted FIM scores derived from the logarithmic formula matched the actual change in FIM scores. The changes predicted the recovery of motor rather than cognitive functions. Regression analysis showed a close fit between logarithmic modelling and actual FIM scores (across-subject R2 = 0.945). CONCLUSIONS: Provided with two initial time-point samplings, logarithmic modelling allows accurate prediction of functional recovery for individuals. Because the modelling is mathematically simple, it can be widely applied in daily clinical practice.

Adult↗
PubMed2005

Alternating hemiplegia of childhood: a study of neuropsychological functioning.

Alternating hemiplegia of childhood (AHC) is a rare chronic neurological disorder characterized by alternating transient attacks of hemiplegia. Evidence from recent studies suggests the disorder is characterized by tonic fits, dystonic posturing, and ocular motor abnormalities. Although widely observed, deficits in cognitive functioning are among one of the least described features of AHC. Most studies describe global deficits, however, no study has provided a comprehensive neuropsychological assessment of a child with AHC. This study presents neuropsychological findings from a comprehensive assessment of a single child with AHC. Results showed significant deficits in intellectual, academic, memory, attention, and executive functioning. Additional deficits in language, psychomotor abilities, and psychosocial functioning were noted. Preliminary longitudinal data are also offered to examine the progressive nature of this disorder. Cognitive strengths and weaknesses are discussed at length as well as recommendations for the classroom and future research.

Child↗
PubMed2003

Widening spectrum of congenital hemiplegia: Periventricular venous infarction in term neonates.

MRI in five term children with congenital hemiplegia without clinically apparent prenatal or perinatal difficulties showed a focal or porencephalic enlargement of the lateral ventricle and periventricular T2 prolongation, which were identical to findings of periventricular venous infarction seen in preterm children. Some cases of congenital hemiplegia in term neonates may be due to clinically silent periventricular venous infarction that occurred in utero.

Cerebral Hemorrhage↗
PubMed2005

Mutation in the glutamate transporter EAAT1 causes episodic ataxia, hemiplegia, and seizures.

BACKGROUND: Transporters, ion pumps, and ion channels are membrane proteins that regulate selective permeability and maintain ionic gradients across cell membranes. Mutations in CACNA1A encoding a neuronal calcium channel and ATP1A2 encoding an ion pump cause episodic ataxia, hemiplegic migraine, and seizures. Mutant gene products of both CACNA1A and ATP1A2 may affect neurotransmission of glutamate, the most abundant excitatory amino acid neurotransmitter. METHODS: We examined our patient population with episodic ataxia and hemiplegic migraine but with no mutation in either CACNA1A or ATP1A2. We looked for mutations in SLC1A3, which encodes the glutamate transporter excitatory amino acid transporter (EAAT) 1 that is important in removing glutamate from the synaptic cleft. RESULTS: A patient with episodic ataxia, seizures, migraine, and alternating hemiplegia has a heterozygous mutation in SLC1A3 that is not present in his asymptomatic parents and controls. Expression studies of the mutant EAAT1 showed decreased expression of the protein with a markedly reduced capacity for glutamate uptake. When coexpressed, the mutant EAAT1 decreased the activity of wild-type EAAT1 but not of two other transporters EAAT2 or EAAT3, suggesting that mutant EAAT1 specifically multimerizes with wild-type EAAT1 to exert its dominant negative effect. CONCLUSION: Our data show that a heterozygous mutation in EAAT1 can lead to decreased glutamate uptake, which can contribute to neuronal hyperexcitability to cause seizures, hemiplegia, and episodic ataxia.

Animals↗
PubMed2006

Small vessel abnormalities in alternating hemiplegia of childhood: pathophysiologic implications.

BACKGROUND: The pathophysiology of alternating hemiplegia of childhood (AHC) is unclear. The authors evaluated the skin and muscle biopsies from patients with AHC for vascular abnormalities. METHODS: Skin biopsy specimens from four patients ages 18 months, 8 years, 9 years, and 18 years and muscle biopsies from two of these patients were examined by electron microscopy and compared with healthy controls. RESULTS: Vascular abnormalities were found in both skin and muscle. Skin biopsies showed similar abnormalities in all four patients. Vacuoles were visible in the endothelium. The most striking abnormality was the presence in the tunica media of small and unevenly shaped vascular smooth muscle cells (VSMCs) containing intracytoplasmic vacuoles and, occasionally, apoptotic nuclei, with variations according to patient age. Moreover, most VSMCs had lost junctions with neighboring cells, and some were completely isolated. In vessels from muscle biopsies, the VSMCs showed vacuoles, residual osmiophilic deposits, and myofilament loss with substitution by vacuoles. CONCLUSIONS: The vascular abnormalities in our patients suggest a primary or secondary vascular pathophysiology to alternating hemiplegia of childhood. The vascular smooth muscle cells may be the initial target of the disease process.

Adolescent↗
PubMed1976

Anosognosia for hemiplegia: somatosensory evoked potential studies.

Somatosensory evoked potential studies in nine patients with anosognosia for left hemiplegia and in one patient with anosognosia for right hemiplegia revealed an absence of response over either hemisphere on stimulation of the median nerve on the hemiplegic side. This apparent lack of cortical processing may underlie the impaired awareness of the hemiplegic side, manifested as anosognosia.

Agnosia↗
PubMed1976

Neurophysiologic changes in hemiplegia. Possible explanation for the initial disparity between muscle tone and tendon reflexes.

In an attempt to clarify the neurophysiologic changes that may follow a cerebral lesion in man, we have studied patients with recent and with long-standing hemiplegia from cerebral infarction. In patients with recent cerebral lesions, inhibition of the monosynaptic reflex by vibration is enhanced. In patients with long-standing cerebral lesions, this inhibitory mechanism is less effective and a comparison of the electrically and mechanically induced monosynaptic reflexes suggests that fusimotor drive may be increased. Related clinical findings are reduced muscle "tone" immediately after the lesion and increased muscle "tone" and exaggerated tendon jerks in patients with long-standing hemiplegia.

Adult↗
PubMed1979

Pyramidal infarction in the medulla: a cause of pure motor hemiplegia sparing the face.

We present a case with an infarct limited to the right pyramidal tract in the medulla. The lesion lay approximately 1 cm below the pontomedullary junction. On the basis of this case and three previously reported cases of medullary pyramidal infarction, there is defined a syndrome of severe hemiplegia with relative sparing of the face, tongue and articulation, minimal sensory loss, and good recovery. The hemiplegia is initially flaccid and later spastic. Transient symptoms, referable to the tegmentum of the medulla, occur at the onset, and reflect ischemia in the deeper territory of a paramedian penetrating vessel.

Brain↗
PubMed1983

Capsular stroke as a cause of hemiplegia in infancy.

Small, deep lesions of the internal capsule are an uncommon cause of infantile hemiplegia. We report the clinical and radiographic findings of three children with hemiplegia with capsular lesions. Although the etiology of capsular stroke in these children remains uncertain, neither hypertension, coagulopathy, nor vascular malformation was an important factor.

Cerebrovascular Disorders↗
PubMed1990

Hemiplegia in posterior cerebral artery occlusion.

We report 4 patients with hemiplegia due to a posterior cerebral artery occlusion. Associated clinical signs were aphasia, alexia or a neglect syndrome, hemianopia, and hemisensory loss. Hemiplegia was due to infarction in the lateral midbrain. The level of the occlusion in the posterior cerebral artery may be located distal to the junction with the posterior communicating artery.

Aged↗
PubMed1991

Reciprocal inhibition between forearm muscles in spastic hemiplegia.

We studied reciprocal inhibition of H-reflexes in the forearm flexor and extensor muscles in 14 patients with spastic hemiplegia secondary to a focal cerebral lesion and 14 normal volunteers. In the spastic limb, the Hmax/Mmax ratio was increased in both flexor and particularly extensor wrist muscles. The 3 normal inhibitory phases of reciprocal inhibition between extensor and flexor forearm muscles were markedly reduced on the spastic side of patients. The early disynaptic phase showed the greatest alteration. Reduced or absent inhibition between forearm muscles associated with increased spinal motoneuron excitability may be typical to spastic hemiplegia.

Brain Diseases↗
PubMed1993

Alternating hemiplegia of childhood: a study of 10 patients and results of flunarizine treatment.

Alternating hemiplegia of childhood is a rare syndrome characterized by onset before 18 months of age of frequent attacks of alternating paralysis, transient ocular palsies, nystagmus, choreoathetosis, and autonomic dysfunction. We describe features of 10 patients followed for up to 27 years. The mechanism of alternating hemiplegia remains unknown but an association to migraine is suspected because of the strong family history of migraine and aura symptoms in some patients. We treated nine patients with flunarizine, a calcium channel blocker, for up to 5 years; they showed a reduction in duration of the hemiplegic attacks, but the episodes ceased completely in only one patient. With long-term follow-up, the persistent motor, movement, and cognitive deficits are more apparent. It is not certain if the flunarizine alters this course.

Adolescent↗
PubMed1994

Benign familial nocturnal alternating hemiplegia of childhood.

In infancy, two brothers developed recurrent attacks of alternating or bilateral hemiplegia arising exclusively out of sleep. The episodes were terminated by even brief sleep. Neither child had hypotonia, dystonic attacks, paroxysmal eye movement abnormalities, or other features characteristic of the now-classic form of alternating hemiplegia of childhood (AHC). The development of the brothers has so far remained normal. Both parents have a history of migraine. In the older boy, magnetic resonance spectroscopy (MRS) of muscle showed increased inorganic phosphate similar to what is found in children with AHC. In the younger brother and parents, MRS of muscle was normal. Other investigations were unrevealing. Flunarizine greatly reduced the duration of attacks. This genetically determined disorder represents a specific entity that is probably migraine-related and is easily misdiagnosed as AHC. Because of its benign course, particularly as far as mental development is concerned, it must be distinguished from classic AHC, which has a terrible prognosis.

Adult↗