Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0018991 (hemiplegia)
 3,997 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Spontaneous cervical epidural hematomas are uncommon lesions that usually produce permanent neurological deficit unless there is early surgical decompression. They are now well-recognized by scan X and especially by sagittal MRI of the spine. We describe 2 patients, a 24 year-old man and a 79 year-old woman with no previous history of trauma who were admitted in emergency for a sudden weakness of limbs, respectively a tetraplegia and a right hemiplegia. Both patients complained of inaugural and acute neck pain. Motor deficit completely resolved in few hours and MRI of the spine showed on T1 a signal isointense, extending respectively from C3 to C6 and C5 to C7, consistent with an hematoma. Laboratory data and angiography were normal. Surgery was recused. Neck pain lasted about a week. Follow-up MRI, in one case, was normal two months later. Cervical epidural hematomas revealed by transient neurological findings that completely and permanently resolved are exceptional. They could mimic ischemic myelopathy and should be considered in the differential diagnosis of other painful vascular conditions like symptomatic vertebral dissection to avoid inappropriate anticoagulation. Conservative management in these cases may be proposed if spontaneous neurological resolution is confirmed by MRI.
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PMID:[Transient neurological manifestations disclosing spontaneous acute cervical epidural hematoma]. 929 66

A 24 year-old woman developed acute hemiplegia and a seizure following accidental catheterization of the right common carotid artery and total parenteral nutrition infusion. Magnetic resonance imaging of the brain showed lesions in the frontal lobe and putamen consistent with an ischemic stroke. Angiography through the central venous catheter confirmed its intra-arterial location. The patient's weakness improved after hyperbaric oxygen treatment. We concluded that stroke or seizures during total parenteral nutrition administration through a central venous catheter should alert one to the possibility of inadvertent intra-arterial infusion, especially in patients who have had central lines inserted several times previously.
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PMID:Hemiplegia caused by inadvertent intra-carotid infusion of total parenteral nutrition. 935 Apr 5

In 1896 Joseph Francois Felix Babinski described for the first time the phenomenon of the toes. In his first paper he simply described extension of all toes with noxious stimulation of the sole of the foot. It was not until 1898 that he specifically described the extension of the hallux with stimulation of the lateral border of the sole. Babinski was probably not aware at the time that E. Remak, a German physician, had previously described the sign. In his third paper of 1903 Babinski concludes that if other authors had described the abnormal reflex before him, they found it fortuitously and did not realize its semiologic value. Babinski probably discovered it by a combination of chance, careful observation and intuition. He also had in mind practical applications of the sign particularly in the differential diagnosis with hysteria and in medico-legal areas. Several of his observations and the physiopathological mechanism proposed by him are still valid today. He realized since 1896 that the Babinski reflex was part of the flexor reflex synergy. He observed that several patients during the first hours of an acute cerebral or spinal insult had absent extensor reflexes. He realized that most patients with the abnormal reflex had weakness of the toes and ankles. He found a lack of correlation between hyperactive myotatic reflexes and the presence of an upgoing hallux. He discovered that not all patients with hemiplegia or paraplegia had the sign. He thought erroneously that some normal subjects could have an upgoing toe. His dream of a practical application of the sign has been fully achieved. The motto of Babinski was Observatio summa lex. Perhaps there is no better dictum in clinical neurology.
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PMID:[100 years of the Babinski sign]. 938 Sep 67

A 32-year-old woman developed chronic progressive hearing impairment, trunkal ataxia, bilateral ptosis and external ophthalmoplegia. She also showed slowly progressive mild to moderate proximal dominant muscle weakness and atrophy. ECG showed incomplete right bundle branch block. An aerobic exercise test showed abnormal blood lactate elevation and muscle biopsy revealed ragged-red fibers in addition to the myopathic change. Analysis of mitochondrial DNA extracted from biopsied muscle and fibroblast samples revealed a 1,758bp deletion from the cytochrome b to ND6 coding regions. Common mutations in tRNALeu(UUR) coding region to the mitochondrial encephalomyopathy, lactic acidosis and stroke-like episodes (MELAS) were not present. She was diagnosed as having incomplete Kearns-Sayre syndrome (KSS). Since the age of 35, she developed complex partial seizure attacks with secondary generalization frequently and at the age of 42, she had a severe generalized seizure with delayed consciousness loss followed by left hemiplegia. MRI showed wide T2-high signal lesions in the right temporo-parieto-occipital area. The proton MR-spectroscopy showed prominent increase of lactate beyond the lesions detected by MRI, indicating diffuse aerobic metabolic dysfunction in the central nervous system. We reviewed two other KSS cases with a stroke like episode, who also had epilepsy and large deletion but no tRNALeu(UUR) mutation, in mitochondrial DNA. Patients with KSS who have seizure may develop the stroke-like episode as seen in MELAS patients.
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PMID:[A case of incomplete Kearns-Sayre syndrome with a stroke like episode]. 940 43

Severe hyperkalemia may cause weakness that typically is ascending and symmetric. In an isolated case report, hemiplegia occurred after the development of hyperkalemia in a patient with a known central nervous system lesion. We describe a patient requiring long-term hemodialysis who had near-fatal hyperkalemia, hemiplegia, and rhabdomyolysis after abuse of crack cocaine. The hemiplegia resolved after normalization of serum potassium using emergency dialysis. No brain lesion could be identified during computed tomography or by electroencephalography, and the patient had no residual neurologic deficits. We conclude that this patient had hemiplegia secondary to cocaine-induced cerebral vasoconstriction because no structural lesion could be found and that the neurologic deficit was worsened by severe hyperkalemia, which probably resulted from cocaine-induced rhabdomyolysis. Hence, despite the absence of a structural lesion of the brain, severe hyperkalemia, typically associated with symmetric, ascending muscle weakness, may contribute to causing focal weakness in the condition of cocaine-induced vasoconstriction.
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PMID:Reversible hemiplegia as a consequence of severe hyperkalemia and cocaine abuse in a hemodialysis patient. 941 48

Although weakness has been identified in cerebral palsy (CP) in isolated muscle groups, the magnitude of weakness in multiple muscles and the patterns of weakness across joints have not been documented. The maximum voluntary contraction of eight muscle groups in the lower extremities of 15 children with spastic diplegia, 15 with spastic hemiplegia, and 16 age-matched peers was determined using a hand-held dynamometer. Children with spastic diplegia were shown to be weaker than age-matched peers in all muscles tested, as were the children with hemiplegia on the involved side, with strength differences also noted on the uninvolved side. Weakness was more pronounced distally in the groups with CP, and the hip flexors and ankle plantarflexors in spastic CP tended to be relatively stronger than their antagonists as compared with the strength ratios of the comparison group. In conclusion, children with spastic CP demonstrate quantifiable lower-extremity weakness and muscle imbalance across joints.
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PMID:Lower-extremity strength profiles in spastic cerebral palsy. 948 98

A 46 year-old woman presented with a weakness of the left side. MRI of the brain showed a left temporal meningioma, a left temporal lobe herniation and two high-signals in the right cerebral peduncle. The involvement of the pyramidal tract in the foot of the cerebral peduncle, in this case, results from temporal lobe hemiation. These findings are different from the mechanisms reported in other cases of ipsilateral hemiplegia. The ipsilateral hemiplegia syndrome was classically described by Ectors in relation to a meningioma of the foot of the third frontal circonvolution. Pathophysiological theories of ipsilateral hemiplegia are reviewed.
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PMID:[Left temporal meningioma disclosed by ipsilateral hemiplegia]. 968 38

An eleven year old boy presented with sudden onset right-sided hemiplegia and ipsilateral lower facial weakness. Two-dimensional echo revealed the diagnosis of idiopathic dilated cardiomyopathy with multiple intracardiac clots. MRI scan of head showed infarctions in the area of caudate nuclei, putamen, brain stem and cerebellum. On anticoagulation therapy, all thrombi, except one, disappeared. The child died 2.5 months later due to resistant cardiac failure.
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PMID:Embolic stroke in a child with idiopathic dilated cardiomyopathy. 971 25

The debate as to whether the sternomastoids receive ipsilateral, contralateral, or bilateral cortical innervation is based largely on the observation of stroke patients and, to a lesser extent, on animal experimentation. The variability of vascular lesions, the lack of pathology correlation in the early reports, and the differences in posture between humans and laboratory animals contributed to the controversy. We studied the function of the sternomastoid (SM) muscles during transient, complete left hemiplegia in 18 right-handed patients undergoing a Wada test. After injection in the right internal carotid artery (ICA), 14 patients were able to lift and turn their heads both to the right and to the left on command. Ten of the 14 patients who were able to follow commands after the injection had weakness of the right sternomastoid compared with the left. Our findings demonstrate that the left hemisphere can activate both the right and the left sternomastoid muscles during suppression of the right hemisphere. The sternomastoids receive bilateral hemispheric innervation and the maximal input comes from the ipsilateral hemisphere.
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PMID:Sternomastoid function during hemispheric suppression by amytal: insights into the inputs to the spinal accessory nerve nucleus. 975 50

We report the case of a 33-year-old woman who developed a dense hemiplegia immediately after an uncomplicated general anaesthetic for diagnostic laparoscopy. She had a history of recurrent hemiplegic migraine with a strong family history. Her migraine was normally associated with visual disturbances and a unilateral headache followed by a left-sided weakness such that she was unable to walk. Symptoms would last up to 24 h. Her post-operative state was atypical of her normal migraine, in that she had no headache or visual disturbance and initially all four limbs were affected.
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PMID:Hemiplegia following general anaesthesia: an unusual presentation of migraine. 978 80


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