Parálisis facial periférica recurrente familiar / Familiar recurring peripheral facial palsy

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Síndrome narcoléptico como posible efecto adverso de paroxetina / Narcoleptic syndrome as a possible side effect of paroxetine

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[Orthostatic tremor induced by pharmaceuticals]. / Temblor ortostático inducido por fármacos.

INTRODUCTION: Dopamine blocking agents can induce gravel types of 'tardive syndromes' (buccolinguomasticatory syndrome, dystonia, akathisia, and less frequently tremor, tourettism, and myoclonus). To our knowledge, orthostatic tremor has not been previously described as a complication of exposure to these drugs. CASE REPORTS: We report four patients who developed orthostatic tremor after exposure to dopamine blocking drugs. Two of them had orthostatic tremor as the predominant but not exclusive type of tremor, and the other two had 'pure' high-frequency orthostatic tremor. Tremor disappeared completely in 3 patients and improved markedly in the other one after gradual withdrawal of the offending drugs (metoclopramide in case 1, sulpiride and thyethylperazine in case 2, and sulpiride in cases 3 and 4). CONCLUSIONS: We propose that this 'tardive orthostatic tremor' could be considered into the spectrum of drug-induced movement disorders.

Temblor ortostático inducido por fármacos / Orthostatic tremor induced by pharmaceuticals

Introducción. Los agentes bloqueadores de los receptores dopaminérgicos pueden inducir distintos tipos de síndromes tardíos (síndrome bucolinguomasticatorio, distonía, acatisia y menos frecuentemente temblor, síndrome de Tourette y mioclonías).En nuestro conocimiento, el temblor ortostático no se había descrito previamente como complicación de exposición a fármacos. Casos clínicos. Presentamos cuatro pacientes que desarrollaron temblor ortostático después de la exposición a agentes bloqueadores dopaminérgicos. Dos de ellos tenían temblor ortostático predominante, pero también otros tipos de temblor, y los otros dos tenían un temblor ortostático `puro' de alta frecuencia. El temblor mejoró claramente en tres de estos pacientes y desapareció por completo en otro al suspender progresivamente el tratamiento con los fármacos señalados (metoclopramida en el caso 1, sulpiride y tietilperacina en el caso 2 y sulpiride en los casos 3 y 4). Conclusiones. Proponemos que el `temblor ortostático tardío' debería considerarse como un trastorno de movimiento inducido por fármacos (AU)

Introduction. Dopamine blocking agents can induce gravel types of ‘tardive syndromes’ (buccolinguomasticatory syndrome, dystonia, akathisia, and less frequently tremor, tourettism, and myoclonus). To our knowledge, orthostatic tremor has not been previously described as a complication of exposure to these drugs. Case reports. We report four patients who developed orthostatic tremor after exposure to dopamine blocking drugs. Two of them had orthostatic tremor as the predominant but not exclusive type of tremor, and the other two had ‘pure’ high-frequency orthostatic tremor. Tremor disappeared completely in 3 patients and improved markedly in the other one after gradual withdrawal of the offending drugs (metoclopramide in case 1, sulpiride and thyethylperazine in case 2, and sulpiride in cases 3 and 4). Conclusions. We propose that this ‘tardive orthostatic tremor’ could be considered into the spectrum of drug-induced movement disorders (AU)

Cefalea inducida por masticación en una paciente con hipertrofia de músculos temporales / Headache induced by chewing in a female patient with hypertrophied temporal muscles

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[Multiple latency test in a patient with episodes of sleep induced by pergolide]. / Test de latencias múltiples en un paciente con episodios de sueño inducidos por pergolida.

OBJECTIVE: Recently, there have been report sleep attacks in parkinsonian patients as a side effect of pramipexole and ropinirole. We report a patient with similar episodes related with pergolide. CASE REPORT: A 64 year old man with rigid akinetic parkinsonism, treated with carbidopa/levodopa and pergolide, developed sudden, irresistible sleep episodes after increasing the dose of pergolide to 2.25 mg/day because of bad control of parkinsonian symptoms. These episodes started 30 minutes after each dose of pergolide and lasted 2 hours. Following reduction of the dose of pergolide to 1.5 mg/day the sleep episodes disappeared. Two double blind multiple sleep latency tests were performed, one after intaking pergolide and other after intaking placebo. RESULTS: The latencies to sleep onset were lower with pergolide than with placebo, but the differences did not reach statistical significance. There was no premature REM sleep onset. CONCLUSION: Sleep episodes are likely a not specific effect of dopamine agonists

Test de latencias múltiples en un paciente con episodios de sueño inducidos por pergolida / Multiple latency test in a patient with episodes of sleep induced by pergolide

Objetivo. Recientemente, se ha comunicado la existencia de ataques de sueño en pacientes parkinsonianos, como efecto secundario de pramipexol y ropinirol. Presentamos un paciente con episodios similares en relación con pergolida. Caso clínico. Varón de 64 años, con parkinsonismo rigidoacinético de 3 años de evolución, en buena situación funcional hasta junio 1999, con arbidopa/levodopa 112,5/450 mg/día y pergolida 1,5 mg/día. En este momento, y justo al aumentar la dosis de pergolida a 2,25 mg/día, el paciente comenzó con episodios súbitos de sueño irresistible, que se iniciaban a los 30 minutos de cada toma de pergolida y duraban dos horas. Tras la reducción de dosis de pergolida a 1,5 mg/día, los episodios de sueño desaparecieron. Se realizaron dos estudios doble ciego de latencias múltiples de sueño, uno tras administración de pergolida y otro tras administración de placebo. Resultados. Las latencias de inicio del sueño fueron menores con pergolida que con placebo, aunque sin alcanzar significación estadística. No hubo comienzo precoz de sueño REM. Conclusiones. Los episodios de sueño o somnolencia diurna excesiva probablemente son un efecto inespecífico de todos los agonistas dopaminérgicos (AU)

Cerebral lymphoma presenting as a leukoencephalopathy.

Cerebral lymphoma is infrequent in immunocompetent patients. This tumour usually appears on CT and MRI as a single lesion or as multiple lesions with mass effect and homogeneous enhancement after contrast administration. A patient is described with a cerebral lymphoma, confirmed by histopathological examination, who presented as a progressive leukoencephalopathy.

Aggravation of glaucoma with fluvoxamine.

OBJECTIVE: To report a case of aggravation of glaucoma associated with the use of fluvoxamine. CASE SUMMARY: A 66-year-old while woman diagnosed with narrow-angle glaucoma showed an increase in intraocular pressure and experienced orbital pain and blurred vision after the initiation of fluvoxamine for tension-type headache. These symptoms disappeared and intraocular pressure normalized after withdrawal of this drug. DISCUSSION: Aggravation of narrow-angle glaucoma is a well-known adverse effect of tricyclic antidepressants. Because this adverse effect had been rarely reported to date with selective serotonin-reuptake inhibitors (paroxetine and fluoxetine), we used fluvoxamine in our patient. The disappearance of ocular symptoms and the normalization of intraocular pressure two days after stopping fluvoxamine suggest a possible relationship between fluvoxamine and aggravation of glaucoma. CONCLUSIONS: Fluvoxamine should be considered as a drug that can induce or aggravate narrow-angle glaucoma.

Pathologic gambling in Parkinson's disease: a behavioral manifestation of pharmacologic treatment?

We describe 12 patients with Parkinson's disease and pathologic gambling. This association has apparently never been reported. The patients were selected from a Parkinson's disease unit of 250 patients. They met Diagnostic and Statistical Manual of Mental Disorders, 4th edition, criteria for pathologic gambling. All patients underwent a neurologic, psychiatric, and psychologic examination, specifically noting the presence or absence of psychopathology in the spectrum of impulse control disorder and the nature of the gambling. Ten patients started gambling after the onset of Parkinson's disease and treatment with levodopa. The pathologic behavior was exclusively present or was markedly increased in "on" periods in 11 patients. All patients had motor fluctuations at the time of the study. Slot machines were the preferred source of gambling for 10 patients, similar to the Spanish gambling population. That the gambling behavior appears more often in the "on" periods of motor fluctuations and that it begins after the onset of Parkinson's disease in most patients and worsens with levodopa therapy suggest that it could be related to the dopaminergic tone in patients with Parkinson's disease and motor fluctuations (that is, it could represent a behavioral manifestation of pharmacologic treatment).

Respiratory chain enzyme activities in spermatozoa from untreated Parkinson's disease patients.

We studied respiratory chain enzyme activities in spermatozoa homogenates from 12 untreated Parkinson's disease (PD) male patients and from 23 age matched healthy male controls. When compared with controls, PD patients showed significantly lower specific activities for complexes I+ III, II+III, and IV. However, citrate synthase corrected activities were similar in patients and controls. Values for enzyme activities in the PD group did not correlate with age at onset, duration, scores of the Unified Parkinson's Disease Rating Scales and Hoehn and Yahr staging. These results suggest that this tissue cannot be used to develop a diagnostic test for PD.

[Respiratory insufficiency as the first sign of mitochondrial disorders]. / Insuficiencia respiratoria como primera manifestación de enfermedad mitocondrial.

INTRODUCTION: In spite of the great variability in clinical signs in the mitochondrial disorders, reports of respiratory disorders in these conditions are purely anecdotal, and almost all occurred in patients with clinical data of the illness. We present a case in which respiratory insufficiency was the first sign of a mitochondrial disorder. CASE REPORT: A 74 year old patient, with no significant clinical history, had two episodes of severe acute respiratory insufficiency without cardiopulmonary causes to justify it. The patient was investigated for neuromuscular disorders and had a muscle biopsy compatible with mitochondrial myopathy. CONCLUSION: The occurrence of respiratory failure in patients with mitochondrial disorders is exceptional, is not related to the degree of deterioration of the respiratory function tests and is potentially reversible.

[Motor and mental complications in the long-term treatment of complicated Parkinson's disease with levodopa]. / Complicaciones motoras y psíquicas en el tratamiento prolongado con levodopa de la enfermedad de Parkinson complicada.

INTRODUCTION: The progression of Parkinson's disease and levodopa therapy leads to development of motor and psychic complications that cause serious limitations to the management of the advanced disease. DEVELOPMENT: This article reviews the current literature regarding the pathophysiology and the therapeutic approaches to the management of motor and psychic fluctuations in Parkinson's disease. CONCLUSIONS: 1. The most important risk factors for the development of motor fluctuations are the young age at onset and severity of Parkinson's disease, and duration and maximum dose of levodopa. 2. Pathophysiological data include the denervation of substantia nigra compacta and postsynaptic pharmacodynamic mechanisms, with a lesser contribution of pharmacokinetic factors. 3. The main therapeutic approaches include changes in the form of administration of levodopa, inhibitors of levodopa catabolism, and dopamine agonists. 4. A number of psychiatric symptoms, including depression, panic attacks, mania and cognitive impairment, can have a fluctuating course, coinciding with the motor fluctuations.

Cerebrospinal fluid levels of selenium in patients with Alzheimer's disease.

We compared CSF and serum selenium levels, measured by atomic absorption spectrophotometry, in 27 patients with Alzheimer's disease (AD) (13 females, 14 males, mean +/- SD age 73.6 +/- 7.4 years) without major clinical signs of undernutrition, and 34 matched controls (18 females, 16 males, mean +/- SD age 70.7 +/- 7.8 years). CSF and serum selenium levels did not differ significantly between AD-patient (11.4 +/- 7.8 ng/ml and 28.5 +/- 13.0 ng/ml, respectively) and control groups (13.3 +/- 7.0 ng/ml and 22.5 +/- 17.5 ng/ml). These values were not correlated with age, age at onset, duration of the disease, and scores of the MiniMental State Examination in the AD group. Weight and body mass index were significantly lower in AD patients than in controls. These results suggest that CSF selenium concentrations are apparently unrelated with the reported oxidative stress processes in patients with AD.

[Pharmacological mechanisms of the treatment of dyskinesias in Parkinson disease]. / Mecanismos farmacológicos del tratamiento de las discinesias en la enfermedad de Parkinson.

OBJECTIVE: The progression of Parkinson's disease (PD) and levodopa therapy leads to development of motor and psychic complications that cause serious limitations to the management of the advanced disease. DEVELOPMENT: This article reviews the current literature regarding epidemiological, clinical, pathophysiological and therapeutics of levodopa-induced dyskinesias (LID). CONCLUSIONS: 1) The most important risk factors for LID are the cumulated doses of levodopa, young age at onset and severity of PD. 2) Pathophysiological data include the nigrostriatal system denervation, the prolonged exposure to levodopa and the integrity of striatal eferences; in addition there are some alterations of dopamine receptors and other neurotransmitter systems. 3) Some pharmacological measures, different for each type of LID, and surgery (pallidotomy, pallidal stimulation, subthalamic stimulation) can be useful for the therapy of LID.