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Biomedical subjects

P I Rosebush

Publications and source records attributed to P I Rosebush.

At least 19 recordsLinked to original sources
PubMed1999

Neurologic side effects in neuroleptic-naive patients treated with haloperidol or risperidone.

OBJECTIVE: To compare the side effect profile of risperidone with that of oral haloperidol in patients with no previous exposure to antipsychotic drugs (APDs). BACKGROUND: Early studies suggested that the APD risperidone may have a side effect profile comparable with that of placebo. These early studies involved patients with chronic schizophrenia and a long history of APD use. Very little information is available regarding the neurologic side effects of risperidone in patients without previous APD exposure. METHODS: The authors prospectively studied 350 consecutive neuroleptic-naive patients admitted to their acute-care psychiatry service; 34 of these were treated with risperidone (mean dose, 3.2 mg/d) and 212 were treated with low-dose haloperidol (mean dose 3.7 mg/d). All patients were assessed on admission and twice weekly thereafter using rating scales for dystonia, parkinsonism, akathisia, and dyskinesia. RESULTS: The incidence and severity of dystonic reactions, akathisia, parkinsonism, and dyskinesia were comparable in the risperidone- and haloperidol-treated groups. CONCLUSIONS: The neurologic side effect profile of low-dose risperidone is comparable with that of haloperidol in patients receiving APDs for the first time. Risperidone may not be a useful alternative to typical APDs for patients with PD and psychosis.

Adult↗
PubMed1999

The neuropsychiatry of adult-onset adrenoleukodystrophy.

Adrenoleukodystrophy is an inherited X-linked peroxisomal disorder that preferentially affects the adrenal cortex, testes, and brain and may occur at almost any age. Psychiatric symptomatology is present in many of the adult-onset cases reported in the literature and may be one of the earliest manifestations of the disease. The majority of patients with psychiatric disturbances have signs and symptoms typical of mania. Psychosis and cognitive impairment may also be prominent. Metabolic diseases such as adrenoleukodystrophy are probably underrecognized as a cause of psychiatric illness. Increased awareness of these disorders will lead to accurate diagnosis, appropriate treatment selection, and genetic counseling.

Addison Disease↗
PubMed1999

Late-onset adrenoleukodystrophy associated with long-standing psychiatric symptoms.

BACKGROUND: It is not commonly appreciated that patients with adrenoleukodystrophy (ALD) can first present in adulthood with psychiatric symptoms. METHOD: This case study involved a 31-year-old man who was referred for a neuropsychiatric assessment of tardive dyskinesia and treatment-resistant psychosis. Upon neurologic examination, he was found to have spasticity, marked hyperreflexia with clonus, and bilateral Babinski signs. T2-weighted magnetic resonance imaging demonstrated severe white matter disease. Metabolic screening revealed abnormalities of very long chain fatty acids consistent with the diagnosis of ALD. These results prompted us to review the literature on late-onset ALD with attention to (1) the nature of the associated psychiatric and neurologic symptoms, (2) the neuroimaging abnormalities associated with this disorder, and (3) treatment considerations. RESULTS: Individuals with adult-onset ALD may initially present with psychiatric symptomatology. Most commonly, these patients manifest signs of mania including disinhibition, impulsivity, increased spending, hypersexuality, loudness, and perseveration. ALD patients will often have upper motor neuron findings on neurologic examination. Despite the name of the disease, patients with ALD may not have clinical evidence of adrenal dysfunction. Neuroimaging reveals diffuse, confluent white matter lesions that typically originate in the parieto-occipital region. Both neuroleptic and anticholinergic medications may result in significant side effects with little resolution of the underlying psychiatric symptoms. CONCLUSION: This case study and review of the literature illustrate the importance of performing neurologic and radiological examinations on all psychiatric patients with chronic illnesses. We emphasize the importance of reexamining and reimaging patients who are not responding to standard treatment. The clinical problem of "treatment resistance" should be seen as an indication that other diagnoses, such as an underlying metabolic disorder, need to be considered.

Adrenoleukodystrophy↗
PubMed1998

Haloperidol induces persistent down-regulation of tyrosine hydroxylase immunoreactivity in substantia nigra but not ventral tegmental area in the rat.

The dopamine antagonist haloperidol can cause tardive side-effects that may persist after the drug is withdrawn. We studied the time course of changes in dopaminergic neurons of the substantia nigra and ventral tegmental area following withdrawal of haloperidol. Rats received daily intraperitoneal injections of saline or haloperidol for eight weeks and were killed at two, four or 12 weeks after the final injection. Sections of substantia nigra and ventral tegmental area were processed for tyrosine hydroxylase immunohistochemistry. Quantitative morphometric analysis was carried out blinded in order to determine the number, cell body size and topography of tyrosine hydroxylase-positive cells, and the immunoreactive area of the substantia nigra and ventral tegmental area. In haloperidol-treated rats, tyrosine hydroxylase-positive cell counts were normal in ventral tegmental area but were decreased in substantia nigra by 34% at two weeks withdrawal and by 52% at four weeks withdrawal; cell counts were almost fully recovered by 12 weeks withdrawal. Cross-sectional area of tyrosine hydroxylase immunoreactivity within the substantia nigra demonstrated a similar pattern of reduction, with full recovery by 12 weeks withdrawal. Mean cell size, by contrast, was essentially unchanged at two and four weeks withdrawal, but was significantly decreased in sub-regions of substantia nigra at 12 weeks withdrawal. These results indicate that haloperidol can produce selective changes in midbrain dopamine neurons that persist long after discontinuation of the drug. This decrease in tyrosine hydroxylase-immunoreactive cell counts may play a role in the neurobiology of the persistent tardive syndromes associated with the use of neuroleptics.

Analysis of Variance↗
PubMed1998

Persistent loss of tyrosine hydroxylase immunoreactivity in the substantia nigra after neuroleptic withdrawal.

A 37 year woman developed neuroleptic induced parkinsonism that persisted long after the drug had been discontinued. This prompted a study of the effect of an eight week course of haloperidol (HAL) followed by two week withdrawal, on dopaminergic neurons of the substantia nigra in rats. Animals treated with HAL showed a highly significant 32%-46% loss of tyrosine hydroxylase (TH) immunoreactive neurons in the substantia nigra, and 20% contraction of the TH stained dendritic arbour. Neuroleptic drug induced downregulation of nigral dopaminergic neurons may help to explain the persistent parkinsonism found in many patients after withdrawal of medication.

Analysis of Variance↗
PubMed1998

Neuropsychiatric aspects of the adult variant of Tay-Sachs disease.

Tay-Sachs disease (a GM2 gangliosidosis) is an inherited neuronal storage disease that can affect individuals across the age spectrum. Psychosis is reported in 30% to 50% of adult-onset patients, and many are misdiagnosed with schizophrenia. Mood disorders are present in more than 25% and cognitive impairment in more than 20%. Treatment of psychosis with neuroleptics may not have a favorable risk/benefit ratio, but treatment with benzodiazepines or electroconvulsive therapy may be efficacious. Metabolic diseases such as gangliosidosis are probably under-recognized as causes of neuropsychiatric illness. Increased awareness of these disorders will lead to accurate diagnosis, appropriate treatment selection, and genetic counseling.

Adult↗
PubMed1996

Catatonia after benzodiazepine withdrawal.

The use of benzodiazepine medication is associated with a variety of acute and well-recognized withdrawal syndromes including anxiety, agitation, insomnia, and confusion. Catatonia has not previously been described. We report five patients who became catatonic after withdrawal of benzodiazepines. All five were older individuals (53-88 years) who had acutely become immobile, mute, and rigid with refusal or inability to eat or drink. Each of the five showed pronounced and rapid improvement after administration of low-dose lorazepam, which has previously been reported to be effective in the treatment of catatonia. Careful review of the records showed that each of the patients had been taking benzodiazepine medication for anywhere from 6 months to 15 years and that it had been rapidly tapered or abruptly discontinued 2 to 7 days before the onset of catatonia. These cases illustrate that severe and potentially life-threatening catatonia can develop in the wake of benzodiazepine withdrawal. Older individuals may be particularly vulnerable to this side effect.

Aged↗
PubMed1996

Circadian pattern of acute, neuroleptic-induced dystonic reactions.

OBJECTIVE: This study examined the timing of acute dystonic reactions in 200 patients taking neuroleptic medication for the first time. METHOD: Two hundred patients received a twice-daily regimen of low-dose neuroleptic. RESULTS: Over 80% of the episodes of acute dystonia occurred between 12:00 noon and 11:00 p.m. The observed circadian variation was not accounted for by sleep, fatigue, or time elapsed from the last dose of medication. CONCLUSIONS: The finding of a diurnal pattern in one of the recognized side effects of neuroleptic medication suggests that the therapeutic efficacy of neuroleptics might similarly vary over the course of the day.

Acute Disease↗
PubMed1995

Late-onset Tay-Sachs disease presenting as catatonic schizophrenia: diagnostic and treatment issues.

BACKGROUND: It is not commonly appreciated that patients with hexosaminidase A deficiency (Tay-Sachs disease) can first present in adulthood with psychiatric illness. METHOD: A 17-year-old non-Jewish male patient was referred with a history of treatment-resistant catatonic schizophrenia. We uncovered coexistent neurologic abnormalities and evidence of cognitive decline. Metabolic screening revealed a severe deficiency of beta-hexosaminidase A. We reviewed the literature on late-onset gangliosidosis with attention to (1) the nature of the associated psychiatric and neurologic abnormalities and (2) the treatment of psychosis in these patients. RESULTS: The patient's catatonia responded promptly to benzodiazepine therapy. Treatment with neuroleptic medication resulted in the rapid development of neuroleptic malignant syndrome. The patient was thereafter maintained on lorazepam with resolution of his acute psychiatric disturbances and unexpected improvement in his neurologic status. CONCLUSION: Patients with hexosaminidase deficiency may first present in adolescence or adulthood with psychiatric illness, particularly schizophrenic-like psychosis. The presence of speech disturbance, gait abnormalities, movement disorders, and cognitive decline may indicate an underlying metabolic disorder. The use of traditional neuroleptics to treat the psychosis in such individuals may produce an unacceptably high risk/benefit ratio. Benzodiazepines may ameliorate the psychiatric and neurologic abnormalities in these patients.

Adolescent↗
PubMed1994

Lorazepam treatment of acute and chronic catatonia in two mentally retarded brothers.

BACKGROUND: Acute catatonia of the retarded type responds rapidly to treatment with lorazepam. There is little information about (1) the efficacy of benzodiazepines in patients with longstanding catatonic syndrome; (2) the effect of longer-term lorazepam therapy in catatonic patients who do not respond to a brief trial of the medication; and (3) the development of catatonic syndromes in family members. METHOD: We gave lorazepam to two mentally retarded brothers with catatonia. One had become catatonic 2 weeks before starting treatment while the other had been hospitalized in a catatonic state for 5 years. RESULTS: The brother with acute catatonia recovered slowly but completely within 2 weeks of starting lorazepam. The brother with long-standing catatonia responded gradually during the first 5 months of treatment and required higher doses of lorazepam but did eventually recover and was discharged from the hospital on a regimen of lorazepam after 1 year of treatment. CONCLUSION: (1) Lorazepam may be effective even in patients who have been catatonic for years. (2) Catatonic patients who do not recover immediately with lorazepam may respond to a longer course or higher doses of the medication. (3) There may be a familial predisposition to developing catatonia in response to stressful situations.

Adult↗