Methanol intoxication. Parkinsonism and decreased Met-enkephalin levels due to putaminal necrosis

Due to methanol intoxication, a 38-year-old male developed permanent parkinsonism with visual impairment. Brain computerized tomography (CT) and magnetic resonance imaging (MRI) revealed cystic resorption of the putamen. An alteration of the central noradrenergic activity and the opioid system can be assumed because of increased dopamine beta-hydroxylase (D beta H) activity and decreased methionine-enkephalin (Met-Enk) levels in the cerebrospinal fluid (CSF).     

A case of delayed myeloneuropathy due to malathion intoxication]

We report a patient with serious organophosphorus-induced delayed neurotoxicity due to malathion. The patient was a 49-year-old male with a history of habitual alcohol drinking, who ingested approximately 100 ml of 50% malathion [S-1,2-bis(ethoxycarbonyl)-ethyl-0,0-dimethyl phosphorodithioate solution], with a large amount of alcohol in a suicide attempt. Following recovery from an acute cholinergic phase 36 hours after ingestion, respiratory muscle weakness, consciousness disturbance and diffuse weakness of the limb muscles occurred, necessitating mechanical ventilation. On the 7th hospital day, glove and stocking type sensory disturbance was observed and weakness of the limbs had progressed to distal dominant flaccid quadriparalysis with moderate muscle atrophy. Two months after onset, neurogenic bladder and spinal automatism became obvious. After 7 months, spasticity of the lower limbs developed, while the weakness of the upper limbs improved. Sural nerve biopsy showed axonal degeneration, loss of large myelinated fibers and increases in Schwann cell clusters. These findings were similar to those seen in patient with triorthocresyl phosphate (TOCP) intoxication. The symptoms of this patient seemed to correspond to Senanayake's "intermediate syndrome". The final clinical features and sural nerve biopsy findings were in close agreement with those in patients with serious organophosphorus compounds induced delayed neurotoxicity due to TOCP intoxication. However, this patient exhibited more severe neuropathy than seen in previously reported cases of organophosphorus compounds induced delayed neurotoxicity caused by less toxic organophosphorus compounds, such as Dipterex. This suggests that alcohol might have been an etiological factor in damage of nervous tissue in this rare case. This is the first case of organophosphorus compounds induced delayed neurotoxicity due to malathion to be reported in Japan.     

Persistent cognitive deficits associated with lithium intoxication: a neuropsychological case description

We present the case of a 51-year-old patient with an acute lithium intoxication associated with several cognitive deficits. During the acute phase of intoxication the patient displayed general psychomotor slowing, dysarthric speech, mood changes, and incoherent discourse. Neuropsychological assessment revealed ideomotor apraxia, profound deficits of visuospatial processing, an impairment of memory and of frontal-executive functions. Other cognitive abilities, such as orientation, spontaneous speech, comprehension, naming, reading, writing, and working memory remained intact. An electroencephalogram revealed diffuse slowing with rhythmic trains, whereas MRI showed no cerebral abnormality. Follow-up examinations at 4 and 14 weeks with lithium levels in the normal range showed substantial recovery of memory abilities and executive functions, whereas praxis and visuoperceptual functions remained impaired, despite the fact that lithium was immediately withdrawn after the intoxication became manifest. We conclude that lithium intoxication may be associated with variable behavioural and cognitive impairments, some of them potentially persistent. Different from other case studies our findings suggest that lithium intoxication may cause a combined, multifocal functional impairment of subcortical and cortical neural mechanisms in both hemispheres.     

Choreoathetosis related to lithium intoxication

A 76-year old woman was admitted because of severe gait ataxia and dysarthric speech that had worsened over the last 24 h. The patient was initially suspected of having repeated transitory ischemic attacks (TIAs) as her daughter reported a similar episode that had happened 3 weeks prior to admission. The onset of spontaneous twisting, choreoathetotic movements of both hands and arms and worsening of symptoms one hour after admission together with a history of lithium therapy lead to the correct diagnosis and appropriate treatment.     

A Creutzfeldt-Jakob like syndrome due to lithium toxicity.

Two patients with lithium toxicity presented with a neurological syndrome suggesting a diagnosis of Creutzfeldt-Jakob disease. In both cases, the initial EEG was consistent with this diagnosis. Neither patient had permanent neurological sequelae and the EEG returned to normal. A careful drug history should be taken in any patient who presents with a rapidly progressive dementia even when the EEG supports a diagnosis of Creutzfeldt-Jakob disease.     

Trigeminal neuralgia due to lengthy AVM treatment. A case report

The authors presented a case of iatrogenic trigeminal neuralgia in a 46-year-old man with a dural arteriovenous malformation (AVM) previously treated by means of intravascular embolization. At first, microvascular decompression (MVD) in the posterior fossa was performed, but unfortunately the pain persisted. Subsequently, percutaneous stereotactic radiofrequency rhizotomy was carried out. The procedure was uneventful and brought about an immediate pain relief.     

Parkinsonism secondary to chronic subdural hematoma. A case report]

We described a case of secondary parkinsonism due to chronic subdural hematoma (CSH). An 83-year-old man developed memory impairment and gait disturbance gradually since one year ago, and these symptoms subacutely deteriorated after he fell down and hit his head. On admission he had moderate cognitive impairment, gait disturbance (wide-based, small steps and initial freezing), postual instability, akinesia and right-sided rigidity. He did not have resting tremor. A CT scan showed a right-sided CSH with marked compression on the left hemisphere, and remarkable decrease of the blood flow in the left cerebral hemisphere was revealed by single photon emission computed tomography. His neurological condition improved gradually through the decrease of the CSH, which suggested the diagnosis of secondary parkinsonism due to CSH. We thought that the CSH in the right hemisphere caused right-sided parkinsonism through mechanical compression to the left hemisphere, which was shown in the SPECT image, in this case. Elderly people suffering from subacute progressive parkinsonism, should undergo CT studies be to differentiate the parkinsonism secondary to CSH.     

Parkinsonism associated with obstructive hydrocephalus due to idiopathic aqueductal stenosis

Two cases of parkinsonism after recurrent obstructivehydrocephalus due to idiopathic aqueductal stenosis are reported.In both patients an extrapyramidal syndrome was noted in the absence ofcontemporaneous evidence of hydrocephalus or shunt failure. One of thepatients underwent a shunt operation, but showed no clinicalimprovement. However, both patients improved after the administrationof dopaminergic therapy. The seven previously reported cases of thissyndrome were reviewed and it is concluded that the prognosis of theparkinsonism is good, usually with total, or near total, resolution. Itis recommended that if a patient with idiopathic aqueduct stenosisdevelops hydrocephalus or evidence of shunt malfunction in associationwith acute parkinsonism their shunt should be replaced. If there is noevidence of hydrocephalus or shunt malfunction they should initially betreated with domaminergic medication.