Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0004134 (ataxia)
 15,886 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

It is suggested that damage by mild trauma, viruses or bone disease to the otic capsule or to the membranes between the cochlea and the middle ear is common, and involved in many syndromes of obscure etiology. The clinical perilymph fistula (PF) syndrome can consist of any combination of the following: tinnitus, deafness, phonophobia, vertigo, ataxia, otalgia, facial palsy, headache, diplopia, blackouts, psychological distress. The following testable hypotheses are proposed: otitis media is due to perilymph in the middle ear, with secondary changes resulting from infection or inflammation: otosclerosis results from a slow leak in the presence of enzymes promoting bone growth: Meniere's syndrome follows reduced perilymph support for the endolymphatic system: Bell's palsy results from a perilymph provoked oedema in the bony facial nerve canal: PFs may be responsible for progressive rubella deafness, and for some cases of migraine, epilepsy, anxiety neurosis and hysteria: psychiatric sequelae of the PF syndrome predominate in the post-concussional syndrome and infantile autism: organisms can pass from the throat into the spinal fluid, causing meningitis or encephalitis. The tinnitus and vertigo are caused by random labyrinthine fluid movements, the headache and diplopia by reduced spinal fluid pressure.
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PMID:Perilymph fistula: a cause of auditory, vestibular, neurological and psychiatric disorder. 78 62

Eight children with recurrent attacks of neurologic dysfunction referable to the brainstem and cerebellum are reported. The episodes occur suddenly, clear completely, and leave the patient without residua. The most frequent signs are ataxia, alternating hemipareses, and vertigo. The majority of patients are girls, and most have the onset of the condition prior to the age of 4 years. Headache was definitely present in three children, and possibly present in four. A striking history of migraine was found in seven families, accounting for 16 affected relatives. Fifteen of these were female and 14 were on the maternal side. Follow-up of the children has not provided any evidence for progressive neurologic disease. The patient followed for the longest period of time has developed classic migraine.
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PMID:Basilar artery migraine in young children. 119 29

Three cases from one kindred who suffer from dominant paroxysmal ataxia are described. This is a rare benign non-progressive disorder of childhood onset, characterised by bouts of ataxia with abrupt onset lasting minutes or hours. Cases may be identified on the basis of a suggestive history, nystagmus persisting between episodes, and dominant inheritance. Treatment with acetazolamide is often dramatically effective. This family is thought to be the first described in the UK but many more probably exist, mislabelled as epilepsy or migraine.
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PMID:Familial paroxysmal ataxia: report of a family. 156 84

Transient recurrent confusional and stuporous states of nonepileptic origin are clearly less frequent than epileptic ones. They are relatively common in diseases of disturbed vigilance, like narcolepsy, idiopathic hypersomnolence, and sleep apnea. These patients often suffer from attacks of hypovigilance, characterized by altered awareness, automatic behaviour and partial or complete amnesia for the attack. Because of the memory 'black outs' and the frequently associated hypnagogic hallucinations, the patients behave inappropriately and often appear confused. Confusional states also typically arise during basilar artery migraine attacks. This special form of complicated migraine predominantly affects young females and is characterized by symptoms and signs of brain stem dysfunction such as vertigo, ataxia, paresthesia, limb weakness, dysarthria; in 75% of the cases, disorders of consciousness dominate. Transient ischemic attacks are sometimes recurrent and, when involving the cranial basilar territory, may result in confusional states without significant motor dysfunction. Attacks of transient global amnesia are possibly also ischemic in nature and are assumed to arise from transient bilateral limbic failure. Affecting only memory functions, they are strictly spoken not confusional, but must nevertheless be taken into consideration when proper observation during the attack was not possible.
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PMID:[Non-epileptic impaired consciousness in neurologic diseases]. 267 60

Four families are described with an autosomal dominant illness characterized by the childhood onset of recurrent attacks of prolonged ataxia, server vertigo, and vomiting. The attacks often begin in infancy. On the average, attacks occur monthly, and last between one hour to more than a week. Variations in severity occur within families. During an attack, consciousness is unaltered, but severe vertigo makes walking impossible and vomiting is frequent and severe. An attack is marked by horizontal and vertical jerk nystagmus, accompanied by vertigo which is sometimes worsened by position; however, there is no muscular weakness. During an attack, blood gases, ammonia, and amino acid studies are normal. Between attacks patients manifest combinations of slight horizontal or vertical jerk nystagmus or mild clumsiness. Cochlear and labyrinthine studies and neurologic investigations were noncontributory. Conventional therapies for vertigo, epilepsy, and migraine were ineffective, but acetazolamide (250-500 mg/day) stopped the attacks.
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PMID:Dominant recurrent ataxia and vertigo of childhood. 350 70

A family with hemiplegic migraine has been documented for a period of over forty years. From this study and the literature we conclude that (1) migraine is a cause of recurrent coma which may be associated with life-threatening cerebral hemisphere oedema; (2) hyperpyrexia with CSF pleocytosis occurs in hemiplegic migraine, which may thus simulate viral meningoencephalitis; and (3) cerebral angiography is hazardous in hemiplegic migraine and may exacerbate coma and cerebral oedema. In the family reported, cerebellar ataxia was present during recovery from attacks of hemiplegic migraine and affected patients ultimately suffered from persistent ataxia with radiological cerebellar atrophy. This syndrome thus constitutes a distinct form of late-onset autosomal dominant cerebellar ataxia and also of familial periodic ataxia. The status of 'cerebellar migraine' is reviewed.
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PMID:Migraine coma. Meningitic migraine with cerebral oedema associated with a new form of autosomal dominant cerebellar ataxia. 404 74

We present four children with benign paroxysmal torticollis (BPT) and a review of the literature. BPT appears to be a self-limited disorder that occurs predominantly in females. The attacks of head tilting usually start in infancy, may recur at varying intervals until the age of 1 to 5 years, and may be confused with other seizures. Other symptoms, such as ataxia and vomiting, may be associated with the attacks of torticollis. Less frequently, infantile migraine also may be associated.
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PMID:Benign paroxysmal torticollis in infancy. 670 34

A mother and son suffer from hemiplegic migraine with onset in childhood. Both have nystagmus which has not changed for many years, but the date of onset is uncertain. They have an asymmetrical tremor, clinically indistinguishable from essential tremor. Neuroophthalmological examination revealed inability to produce smooth pursuit, gaze-paretic nystagmus, rebound nystagmus, failure of fixation suppression of the vestibuloocular reflex both horizontally and vertically, and low gain of the optokinetic system. These abnormalities, confirmed by electrooculography, are commonly seen in disease of the cerebellum and brainstem. Treatment with propranolol and pizotyline lessened the number of episodes of hemiplegia and improved the tremor. Hemiplegic migraine has been reported in association with nystagmus, retinal degeneration, deafness, and ataxia in varying combinations in three other families with autosomal dominant inheritance. These associated neurological manifestations likely represent system degenerations rather than the effect of repeated ischemia imputable to the migraine itself. The syndrome of hemiplegic migraine, tremor, and ocular smooth pursuit system disorder seen in this family appears to be inherited as a single autosomal dominant trait, although more than one autosomal dominant gene may be involved.
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PMID:An autosomal dominant syndrome of hemiplegic migraine, nystagmus, and tremor. 743 78

Eight patients with the syndrome of benign paroxysmal vertigo of childhood are presented. This symptom complex is characterized by attacks of vertigo in young children combined with nystagmus, ataxia and transiently decreased vestibular function, but without impaired consciousness. Diagnostic and follow-up studies revealed a close relationship to other forms of autonomic nervous system instability, particularly to the migraine symptom complex.
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PMID:Benign paroxysmal vertigo of childhood: a migraine equivalent. 743

A 55 year old woman with multiple sclerosis presented with a 5 week history of an exacerbation of symptoms. Prominent among these symptoms was trigeminal neuralgia, migraine headaches, blurring of vision, and ataxia of gait. While treatment with carbamazepine (TegretolR) (800 mg/d) and oral prednisolone (15 mg/d) over a 4 week period produced no improvement in symptoms, externally applied magnetic fields (MF) (7.5 picoTesla; 5 Hz) placed over the scalp for a 7 minute period on three different days resulted in a complete resolution of symptoms within two weeks of initiation of treatment. Partial relief of the neuralgic pain and headaches was obtained immediately after completion of the first treatment indicating that resolution of symptoms was related to the effects of MF and not to a spontaneous remission. This is the first report demonstrating the clinical efficacy of pico Tesla range MF in rapidly resolving an acute relapse of MS.
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PMID:Successful treatment of an acute exacerbation of multiple sclerosis by external magnetic fields. 808 29


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