What can man do without basal ganglia motor output? The effect of combined unilateral subthalamotomy and pallidotomy in a patient with Parkinson's disease.

We have studied motor performance in a man with Parkinson's disease (PD) in whom thermolytic lesions of the left subthalamic and left globus pallidus nuclei interrupted the basal ganglia (BG)-thalamo-cortical motor circuit in the left hemisphere. This allowed us to study remaining motor capabilities in the absence of aberrant BG activity typical of PD. Movements of the left arm were slow and parkinsonian whereas movement speed and simple reaction times (RT) of the right (operated) arm were within the normal range with no obvious deficits in a range of daily life activities. Two main abnormalities were found with the right hand. (a) Implicit sequence learning in a probabilistic serial reaction time task was absent. (b) In a go/no-go task when the percent of no-go trials increased, the RT superiority with the right hand was lost. These deficits are best explained by a failure of the cortex, deprived of BG input, to facilitate responses in a probabilistic context. Our findings confirm the idea that it is better to stop BG activity than allowing faulty activity to disrupt the motor system but dispute earlier claims that interrupting BG output in PD goes without an apparent deficit. From a practical viewpoint, our observations indicate that the risk of persistent dyskinesias need not be viewed as a contraindication to subthalamotomy in PD patients since they can be eliminated if necessary by a subsequent pallidotomy without producing deficits that impair activities of daily life.

[Status epilepticus]. / Status epilepticus.

Status epilepticus (SE) is one of the most important neurological emergencies. We describe the most recent aspects concerning the definition, classification, aetiology, physiopathological and epidemiological aspects of SE, together with the therapeutic principles and pharmacotherapy in adults and adolescents. The therapeutic control of SE becomes more difficult as its duration becomes longer, and the possibility of causing permanent neurological damage also increases. Treatment is more effective when it is performed following a protocol. The benzodiazepines are still a first line of treatment. Home care treatment of patients with recurring seizures or important risk factors for developing SE could help to improve the future response to therapy and, therefore, its prognosis. Thus, several therapies involving benzodiazepines are developed which can be administered rectally, nasally and sublingually. In the future, treatment may include the use of neuroprotective drugs that reduce the morbidity and mortality of SE and prevent cell death. In spite of the progress made in understanding SE, there are still certain shortcomings that must be solved, i.e. mistakes made during diagnosis, a need for wider availability of electrographic controls, the basic physiopathological mechanisms require further research, and controlled studies with currently available antiepileptic drugs and others that have only recently appeared should be conducted in order to evaluate their therapeutic effectiveness, in both home care and hospitalised patients (refractory SE).

Drug-induced parkinsonism in a movement disorders unit: A four-year survey.

UNLABELLED: To establish the frequency of drug-induced parkinsonism (DIP) and the drugs responsible for this side-effect we reviewed the database of our Movement Disorders Unit during the first 4 years of its use. The diagnostic criteria for DIP included: (1) the presence of two or more cardinal symptoms of parkinsonism, (2) an absence of parkinsonian symptoms before the exposure to the offending drug, (3) a disappearance or significant improvement in parkinsonism after withdrawal of the offending drug, (4) no better explanation for the parkinsonism. One-hundred and five patients fulfilled the diagnostic criteria for DIP (16.3% of total patients referred and 33.8% of patients with parkinsonian syndromes). Drug-induced parkinsonism was related to 1, 2, 3, 4, 5 and 7 drugs in 62, 30, 9, 1, 2 and 1 patients, respectively. The most frequently offending drugs were: calcium-channel blockers (61 cases), antipsychotic drugs (29 cases), thiethylperazine (18 cases), clebopride (14 cases), and sulpiride (10 cases). When compared with idiopathic Parkinson's disease patients, DIP patients were predominantly female and showed an older age at the onset of parkinsonian signs. Parkinsonian signs only disappeared completely in 41 patients (39.0%). IN CONCLUSION: (1) DIP was a frequent cause of parkinsonism in our Movement Disorder Unit, (2) calcium-channel blockers, and/or orthopramides and substituted benzamides were a frequent cause of DIP in our series, (3) old age and the female gender were frequent among DIP patients, (4) DIP is not always reversible.

Progressive multifocal leukoencephalopathy in HIV infection presenting as Balint's syndrome.

We report a patient with AIDS presenting with Balint's syndrome. CT and MRI showed the characteristic lesions of a progressive multifocal leukoencephalopathy, which was confirmed by histologic examination.

Chronic paraparesis associated with human T-lymphotropic virus type I beginning after dental extraction.

We report a patient with a chronic paraparesis associated with human T-lymphotropic virus I infection (HTLV-I antibodies were present in blood and CSF), which began after a dental extraction. We suggest the possible relation of the dental procedure with the triggering of the disease.

Parkinsonism unmasked by verapamil.

We report the case of a 55-year-old man who had a parkinsonian syndrome unresponsive to levodopa for 5 years and had been taking verapamil during the past 8 years. Parkinsonian signs improved markedly after withdrawal of verapamil, suggesting its role in unmasking the parkinsonism. To our knowledge, this side effect of verapamil has not been described previously.