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Query: UMLS:C0036341 (schizophrenia)
 60,220 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We describe a case of clozapine-induced seizures in a patient with treatment-resistant schizophrenia. She had previously been treated unsuccessfully with a number of atypical antipsychotic medications, before she was eventually started on clozapine. She experienced two separate episodes of observed fits whilst on an initial daily dose of 125 mg and, subsequently, on a daily dose of 237.5 mg. Following discontinuation of clozapine, she was rechallenged and again was observed to have seizures. Appropriate investigations ruled out any organic cause of the fits and clozapine was successfully restarted, together with sodium valproate. By the time of treatment stabilization, the patient had not experienced any further fits. These findings suggest that clozapine-induced seizures can be successfully treated, that gradual dose titration can reduce the likelihood of further episodes of seizures and that concomitant use of a suitable mood stabilizer/anti-epileptic medication can improve the outcome of treatment-resistant schizophrenia. Furthermore, the concomitant use of fluoxetine and clozapine is discouraged, with citalopram suggested as a suitable antidepressant in those depressed patients receiving clozapine.
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PMID:A case of clozapine-induced tonic-clonic seizures managed with valproate: implications for clinical care. 1567 Nov 34

Treatment-resistant schizophrenia presents a particular problem in patients who, for whatever reason, cannot be treated with clozapine. Pharmacological strategies for the further management of such individuals usually involve the coadministration of two or more antipsychotic drugs, leading to an increased potential for adverse effects. Hyperprolactinaemia (elevation of serum prolactin levels) is a common side-effect of antipsychotics and one that it is especially important to minimize in patients with primary pituitary pathology. We present a patient with treatment resistant schizophrenia and a prolactin-secreting microadenoma of the pituitary who was intolerant of clozapine therapy. She was prescribed a combination of olanzapine and quetiapine and experienced almost complete resolution of her psychosis, with no elevation of serum prolactin levels. We suggest that this may be a strategy worthy of consideration in patients for whom conventional treatment methods have failed, particularly those who are sensitive to the prolactinogenic effects of many antipsychotic medications.
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PMID:Successful treatment of refractory schizophrenia with combined olanzapine and quetiapine in a patient with a prolactin secreting pituitary microadenoma. 1567 Nov 35

Environmental reduplication or reduplicative paramnesia is one of the content-specific delusions (CSD) which is characterized by reduplication of places. CSD has been reported in focal and diffuse cerebral disorders. A focal lesion such as frontal lobes and the right hemispheric lesion have been documented The authors describe a 66 year-old woman who had a delusion of misidentification for place one month after right middle cerebral artery occlusion. The patient did not have any history of schizophrenia or other psychiatric diseases. The patient believed that her car, furniture and house were duplicated. She also mentioned that her son and friends tried to takeover all of her properties and told everyone that she was insane. The prominent cortical signs were tactile and visual neglect. Neuropsychological assessments revealed poor attention but she had neither confusion nor dementia. Clock drawing and construction tests revealed visuospatial impairment which was compatible with non-dominant hemispheric abnormality. MRI showed evidence of cerebral infarction in the right middle cerebral artery territory. Only one similar patient who had an intracerbral hematoma of the right frontal lobe has been reported in the literature. The role of occipito-parietal and fronto-temporal lobes or their connections in environmental reduplication is proposed.
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PMID:Environmental reduplication in a patient with right middle cerebral artery occlusion. 1582 53

A 19-year-old woman with a 3-year history of schizophrenia suddenly began to vomit, and rapidly developed a coma an hour after the onset of vomiting. A brain CT scan showed diffuse brain edema with compression of the ventricles. Laboratory tests showed a low serum sodium concentration of 117 mmol/L. She died 67 h after the onset of the first symptom. A postmortem examination showed diffuse swelling of the brain with bilateral uncal and tonsillar herniations. Histologically, no necrotic, hemorrhagic or encephalitic changes were seen. However, microvacuolar changes with lymphocytic infiltration were found in the venous walls (media and adventitia) mainly in the basal ganglia, thalamus and brainstem. To our knowledge, this is the first demonstration of venous alterations in fatal hyponatremic brain edema. These changes may have participated in the exacerbation of the brain edema due to functional disturbance of venous drainage.
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PMID:Peculiar venous lesions in fatal hyponatremic brain edema. 1582 24

A 54-year-old woman with schizophrenia presented to hospital with unconsciousness, fever and marked muscle rigidity. She had been given fluphenazine decanoete 20 mg intramuscularly 15 days before the admission and she had continued taking haloperidol 20 mg daily and oral biperiden 2-4 mg. She was extremely rigid and unresponsive. On laboratory investigations revealed: serum sodium 120 mEq/l, creatinine phosphokinase 12,980 IU/l (normal up to 170), lactate dehydrogenase 1544 IU/l (150-500), free trioidothyronine < 1.00 pg/ml (1.5-4.5), free throxyine 0.76 ng/dl (0.8-1.9), thyroid stimulating hormone 1.14 microU/ml (0.4-4), cortisol (at 8.00 a.m.) 9 microg/dl (5-25). Antipsychotic drugs were withdrawn after admission. A diagnosis of secondary adrenal insufficiency and secondary hypothyroidism was made. Hormonal substitution with hydrocortisone and levothyroxine and correction of hyponatremia with intravenous hypertonic saline solution resulted in rapid improvement of symptoms and signs. It seems that the symptoms and signs of hypothyroidism and hyponatremia were attributed to acute psychosis in this patient. As a conclusion failure to recognize the endocrinopathy may not only produce recovery difficulties but also psychiatric and endocrine repercussions if psychotropic medications are given in such masked cases.
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PMID:Possible malignant neuroleptic syndrome that associated with hypothyroidism. 1592 37

Neuroborreliosis has become the most frequently recognized tick-borne infection of the nervous system in Europe and the United States. In addition to dermatological, cardiac, articular, and neurologic manifestations, psychiatric disorders such as depression, panic attacks, and schizophrenia-like psychosis can also arise. We report on a 61-year-old woman who developed a severe pain syndrome following several tick bites. She was diagnosed with neuroborreliosis; she received various courses of antibiotics over several years, but without any clinical improvement in her condition. Her eventual admission to a psychiatric ward due to mental symptoms and neuroleptic treatment led to a dramatic improvement of her pain symptoms. However, increasing delusions disclosed a psychotic episode, which ceased over time. We discuss therapeutic difficulties and psychiatric complications in the absence of a clear-cut diagnosis of neuroborreliosis. Although this patient might have suffered from late-onset schizophrenia with painful hallucinations right from the start of her disease, the case highlights psychiatric complications that might be associated with neuroborreliosis.
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PMID:Painful hallucinations and somatic delusions in a patient with the possible diagnosis of neuroborreliosis. 1595 56

This is a case report of a 56-year-old lady who was admitted to a psychiatric ward because she was showing a plethora of positive and negative symptoms of schizophrenia. She has a positive history of mental illness; her mother had a diagnosis of schizophrenia. The patient did not have any medical history of relevance and was not taking any medication. She was commenced on Aripiprazole and after 5 weeks developed disabling extra-pyramidal side effects. On discontinuation of Aripiprazole, the side effects subsided and disappeared quickly. According to the authors' knowledge, this is the first case of a patient developing extra-pyramidal side effects following treatment with Aripiprazole, not previously exposed to other antipsychotic, and with no co-morbid medical conditions. The authors suggest titrating Aripiprazole slowly.
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PMID:A case of Aripiprazole and extra pyramidal side effects. 1640 61

We report a case of a right-handed, 73-year-old woman with auditory hallucinations lateralized to the right ear. A brain MRI revealed a small infarction in the left dorsomedial nucleus (DM) of the thalamus. The patient did not have either psychiatric or neurological prior history, and had otherwise been treated for ischemic heart disease, hypertension, and hyperlipidemia for 10 years. Two months prior to admission, she had become forgetful, and had lost her wallet several times. She concurrently began to experience auditory hallucinations in which she heard the voices of her acquaintances, or "the gods". She frequently monologized and wandered about outside following the contents of the hallucinations. Therefore, she was admitted to our institution. On admission, no apparent abnormalities were revealed by physical examinations or blood analyses. She was alert and had no aphasic symptoms. Except for memory disturbances, no neurological symptoms, including no hearing loss, were found. A brain MRI showed a small localized infarction in the left DM, but EEG findings were normal. The patient had prominent anterograde memory deficits: she hardly remembered what she had done the very same day, or the names of the doctor and hospital. She also demonstrated a retrograde amnesia of the past decade or two: she showed difficulty recalling either personal history or social events that occurred during this era. Wechsler Adult Intelligence Scale-Revised (WAIS-R) revealed a total IQ of 75 (verbal IQ 77; performance IQ 77). The verbal hallucinations continued with frequent occurrence even after admission. They included voices telling her about misfortunes, such as death or sickness, of her relatives. These turned into threats and commands, such as "I'm gonna kill ya. I attack you from behind. You, do not eat!" In addition, she occasionally experienced "third person auditory hallucination", in which several men were discussing the plan to kill her. As is characteristic of this type of case, the hallucinations always appeared in only her right ear. They did not occur in the other modalities (e.g. as a visual one). She was convinced that the hallucinations were real and looked frightened while they were happening. Whereas the anterograde amnesia continued for 6 months after admission, the retrograde amnesia gradually improved within 2 or 3 months after admission, although a partial amnesia on the past decade eventually turned out to persistent. On the other hand, the hallucinations did not ameliorate satisfactorily with risperidone (3-6 mg/day), but on augmentation with olanzapine (5-20 mg/day), they lessened gradually and almost disappeared within 6 months. She also slowly developed symptoms similar to those of frontal lobe syndrome, i.e., aspontaneity and apathy. In conclusion, our case indicates the importance of DM on memory function. It is noteworthy that schizophrenia-like hallucinations developed in the case. Localized neuronal deficits evoked by infarction in the left DM probably caused the schizophrenia-like hallucinations; the lateralization phenomenon further indicates the involvement of specific neuronal mechanisms in the mediation of the hallucinations. According to the knowledge of the functional anatomy of the DM and the lateralization phenomenon of auditory hallucinations, it is possible that the neuronal loop, comprised of the prefrontal cortex and thalamus, designated as "basal ganglia-thalamocortical circuits", in addition to the left temporal cortex, plays an important role in the development of the hallucinations in this case. This possibility might also shed light on the neurological basis of schizophrenia.
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PMID:[A case of left dorsomedial thalamic infarction with unilateral schizophrenia-like auditory hallucinations]. 1653 98

We describe a patient who was ill for more than 15 years. She was treated predominantly as a neurological case because of multiple motor signs. The diagnosis of catatonia was considered at the time when she was hospitalized in a psychiatric hospital after a suicidal attempt. The "therapeutic blindness", which was obviously present during 15 years of her illness, is discussed: the ICD--10 is perhaps misleading regarding this diagnosis while it associates it too tightly only to schizophrenia.
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PMID:Reappearance of catatonia. A case report. 1664 80

Gilbert's syndrome (idiopathic unconjugated hyperbilirubinemia) is a benign hyperbilirubinemia found in the general population. We report one case in which the exacerbation and remission of hyperbilirubinemia closely correlated with the psychosis of schizophrenia. Some studies have reported that schizophrenic individuals had a significantly higher frequency of hyperbilirubinemia than patients suffering from other psychiatric disorders and the general healthy population. Stress and fasting are well-known contributors to elevated plasma bilirubin levels in patients with Gilbert's syndrome. A 38 year old woman inpatient with acute schizophrenic symptoms had a bilirubin plasma level of 2.7 mg/dl. She was treated with risperidone that produced no adverse effects on hepatic function. Schizophrenic symptoms improved and a decrease in bilirubin plasma concentration was observed.
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PMID:[Gilbert's syndrome and schizophrenia]. 1673 95


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