Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0085631 (agitation)
 12,064 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A 33-year-old man was prescribed amfepramone 75 mg o.i.d. for the treatment of obesity. One week after onset of therapy, he suddenly became agitated and aphasic for several h. A CT scan of the brain was normal. Amfepramone was discontinued. Three days later, there was a second period of agitation and aphasia with a discrete right hemiparesis lasting 12 h. A repeat CT scan and a MRI of the brain were normal. On EEG and brain mapping, alpha-activity was absent over the left hemisphere and a left fronto-temporal delta-focus was found. A Tc-99m HMPAO brain SPECT showed a severe hypoperfusion of the left hemisphere. The next day, the neurological examination was completely normal. Two weeks later, EEG and SPECT had completely normalized. Transient ischemic attacks due to vasospasm were considered to be the most probable clinical diagnosis.
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PMID:Transient ischemic attacks associated with amfepramone therapy: a case report. 814 62

A case of brain stem cavernous angioma associated with peduncular hallucination is reported. A 68-year-old man was admitted with complaints of left sensory disturbance. On the evening of the first hospital day, he developed vividly formed hallucinations. The hallucinations were accompanied by sleep disturbance and agitation. At approximately 2:00 am, he began to feel as though he could see his daughter watching television in a room. At one point he saw vivid pictures. MRI revealed a round mass with a mixed signal intensity core surrounded by a low signal intensity rim in the right brain stem. On the 10th hospital day, there were no hallucinations. On October 12th suboccipital craniectomy was performed and cavernous angioma and the surrounding hematoma was partially removed. Soon after that the patient was discharged with improvement of both ocular movement and left-sided sensory disturbance.
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PMID:[Peduncular hallucination in brain stem cavernous angioma: a case report]. 825 80

Involvement of the central nervous system associated with SLE (CNS lupus) is not rare. Two types of CNS lupus are noted clinically; one group manifesting focal neurological symptoms and another group showing mental symptoms. Though it is well known that neurological symptoms are caused by arteritis and thrombus, pathophysiological mechanisms leading to mental symptoms remain obscure and there is no established clinical evidence responsible for these symptoms. A 41-year-old woman was confused and her attention was markedly impaired. Her mental symptoms consisted of disorientation, restlessness, euphoria and emotional incontinence. There were neither focal neurological signs nor meningeal signs. Cerebrospinal fluid (CSF) examination showed increased number of polymorphonuclear cells and permeability of the blood-brain barrier, calculated based on the CSF/plasma protein ratio, was also elevated. Repeated bacteriological examinations revealed to be negative. Gd-DTPA MRI demonstrated diffuse enhancement of the cerebral leptomeninges. Methylprednisolone pulse therapy ameliorated her mental deterioration effectively, and subsequently the leptomeningeal enhancement with Gd-DTPA MRI disappeared in parallel. These radiological and laboratory findings suggest that SLE itself causes inflammation of vessels in the leptomeninges and adjacent cerebral cortex. We consider mental symptoms associated with SLE may be caused, at least in part, by this mechanism. To our knowledge, we could not find similar reports in the literature. Gd-DTPA enhanced MRI seems to be of clinical use for making diagnosis, evaluating clinical activity and understanding of CNS lupus.
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PMID:[Leptomeningeal abnormality on Gd-DTPA enhanced MRI in a case of SLE presenting diffuse organic brain syndrome]. 833 80

Gradually progressive memory loss is the keystone of Alzheimer's disease (AD). Other diagnostic signs include deterioration of language and perception, judgment losses, and behavioral problems such as agitation and paranoia. The clock drawing test is a simple in-office measure of spatial orientation. CT or MRI is recommended to rule out vascular injury; blood tests can exclude other types of dementia. Serial mental status exams can document disease progression. Drug therapy is appropriate for managing mental symptoms, including early depression and anxiety. Some patients may derive benefit from tacrine. Management must also include education and support of the AD patient's caregivers.
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PMID:New Alzheimer's drug expands your options in symptom management. 833 40

We examined records of sedations provided by the paediatric anaesthesiology staff for 455 children (ages 1 mo-17 yr) undergoing MRI or CT scans at our institution over a twelve-month period with regard to the monitoring of adverse events: excessive sedation, agitation, vomiting, hypoxaemia, and major airway compromise. One hundred-and-thirty-one patients (29%) received chloral hydrate; 324 patients (71%) received propofol. All patients were monitored with continuous noninvasive pulse oximetry and received supplemental oxygen via nasal cannulae. Of the patients who received chloral hydrate, 64 (49%) were over one year of age; of the patients who received propofol, 318 (98%) were one year of age or older. In the chloral hydrate group, 23 patients (19%) were deemed excessively sedated and four patients (3%) were agitated; no patients in the propofol group experienced any of the adverse outcomes reviewed. Furthermore, no patients in either group had significant airway compromise and none was admitted to the hospital as a result of the sedation.
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PMID:An audit of adverse events in children sedated with chloral hydrate or propofol during imaging studies. 859 70

Restlessness and agitation are commonly reported early sequelae of traumatic brain injury (TBI). Severe restlessness (akathisia) is also observed in psychiatric patients as a result of the use of dopamine receptor blocking agents. A recent case study described akathisia in a patient with bilateral orbitofrontal lesions following TBI. We report a case of unusually marked motor restlessness (akathisia) following TBI in a 17-year-old woman. When admitted for rehabilitation she was alert but agitated, severely restless, and mute. She constantly paced her room and the hospital unit, repeatedly retracing the same route. MRI scan revealed large, well-delineated bifrontal contusions. During baseline evaluation prior to anticipated psychopharmacological intervention her restlessness began to resolve rapidly. She became verbal and oriented within expected limits without medication. This case lends support to the observation that akathisia is related to lesions of the prefrontal cortex.
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PMID:Akathisia resulting from traumatic brain injury. 883 18

We report a 83 year-old woman with dementia. She was apparently well until December of 1993 when she was 81-year-old. At that time, she was operated or her cataract. Her post operative course was uneventful, however, shortly after her operation, she had an onset of memory loss and abnormal behavior. She showed a fluctuating course in her mental disturbance. In 1995, her dementia worsened with nocturnal agitation. She was admitted to our service on June 12, 1995. She was alert and her blood pressure was 140/100 mmHg. She showed recent memory loss and disorientation to time. Motor wise, she was unable to stand unsupported. Her gait with support showed small steps and a wide base. She was bradykinetic and ataxic in her finger-to-nose and heel-to-knee test, however, no rigidity or tremor was noted. Her MRI showed T2-high signal lesions in both medial thalamic areas, in the right occipital lobe, and in the bilateral cerebral white matters as well as in the basal ganglia. She was discharged for out-patient follow up on July 3, 1995. Four days after the discharge, she showed declining responses to stimuli and she developed dyspnea on July 14, 1995. She was admitted again on the same day. Her body temperature was 38.5 degrees C and moist rales were heard in the left lung field. She appeared drowsy and no verbal response was obtained; no apparent motor palsy was noted. Blood count showed leukocytosis (14,300/ml). Blood gas analysis under 61 of oxygen inhalation through a mask was as follows: pH 7.460, PCO2 39.6 mmHg, PO2 67 mmHg, and HCO3-28.5 mEq/l. Two days after admission, she developed a convulsion in her left arm and she became unconscious. Her EEG showed periodically recurring lateralized epileptic discharges on the right fronto-central areas. Her subsequent course was complicated by status epilepticus and respiratory distress. She died on July 26, 1995. She was discussed in a neurological CPC. The chief discussant arrived at a conclusion that she suffered from multi-infarct dementia. Bilateral thalamic infarctions were considered to have played a significant role in her dementia. Post-mortem examination revealed subcortical leukoencephalopathy of Binswanger's type and cerebral infarctions in the thalamic and basal ganglia regions and in the right occipital lobe. In addition, she showed isolated angitis of the central nervous system involving mainly in the small arteries located in the superficial areas of the brain and the spinal cord. This patient was interesting in that despite relatively mild leukoaraiosis in MRI, post-mortem examination revealed profound pathologic changes in the subcortical white matters. In addition, she showed the isolated angitis of the CNS. The cause and the clinical correlates of her angitis were unclear.
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PMID:[A 83 year-old woman with dementia, gait disturbance, and convulsion]. 904 33

Thyrotropin (TSH-)producing adenomas of the anterior pituitary gland are the least frequently encountered ones and constitute a very rare cause of hyperthyroidism. The case is presented of a 58 year old male patient with a well-known history of hyperthyroidism over a period of at least 9 years growing goiter. Despite different forms of medical treatment he presented a constant clinical pattern consisting of restlessness and paroxysmal tachycardial atrial fibrillation. Laboratory findings revealed elevated levels of circulating thyroid hormones despite inadequately high levels of TSH. MRI scan revealed an adenoma of the pituitary measuring 9 mm in diameter. After microsurgery, consisting of transphenoidal resection of the tumor, the patient recorded no clinical symptoms. Histological examination revealed positive immunohistochemical staining, with antibodies to TSH, but a negative reaction against the GH, PRL, FSH, LH and ACTH hormone antibodies. Moreover, the levels of circulating hormones (GH, PRL, FSH, LH and ACTH) were normal. TSH-alpha subunits were not elevated. Before the correct diagnosis was reached, this patient was treated for nine years with antithyroid drugs. Five months after the operation the patient showed normal values of circulating thyroid hormones and TSH and thus no thyroid-specific medication was necessary.
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PMID:[Hyperthyroidism caused by TSH producing hypophyseal adenoma]. 922 5

A 53-year-old man presented with progressive ataxia two and a half years prior to admission. Initially he was treated in a local hospital for 4 months with a diagnosis of spinocerebellar degeneration. Subsequently he developed psychomotor excitement with hallucination and was admitted to a mental hospital for 7 months with a diagnosis of Wernicke's encephalopathy. After a year of partial remission, he presented with increasing difficulty in thinking and walking. On admission he developed mental agitation and excitement, ocular flutter and opsoclonus, and prominent cerebellar ataxia. A lymphocytic pleocytosis in the CSF and a high-intensity lesion in the superior cerebellar peduncle of the upper brainstem revealed on a T2-weighted MRI led to a diagnosis of brainstem encephalitis. Treatment with steroid (two series of 3 days of 1,000mg methylprednisolone DIV, followed by 60mg oral prednisolone) brought about a dramatic improvement in mental and ocular symptoms corresponding with the CSF findings. He was left with mild cerebellar ataxia and returned to work on a small dose of steroids. Differential diagnoses including Bickerstaff's encephalitis and pathomechanism were discussed.
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PMID:[Steroid responsive chronic brainstem encephalitis featuring mental symptoms, abnormal eye movement and cerebellar ataxia]. 923 54

We report a 45-year-old man with monocytosis and right hemiparesis. The patient suffered from an acute myocardial infarction from which he recovered completely when he was 42 years old. One year prior to his death, he was found to have increase in monocyte count (35.5% of leukocytes) in peripheral blood and splenomegaly; he was admitted to the hematology service of our hospital. He was diagnosed as having chronic myelomonocytic leukemia after bone marrow examination. He was treated with radiation therapy with improvement in splenomegaly. In May of 1995, he had fever, anemia, and thrombocytopenia for which he needed daily blood transfusion. In November of 1995, he had an onset of weakness in his right hand, and neurologic consultation was asked for in November 27, 1995. Neurologic examination revealed a chronically ill japanese man in no acute distress. He was alert and not demented. Higher cerebral functions were intact. Cranial nerve examination revealed right facial paresis of the central type. Motor-wise, he was right hemiparetic. Generalized muscle wasting was noted apparently due to the chronic debilitating disease. Deep tendon reflexes were within normal range in the right upper extremity, but were diminished in other areas. Sensation was intact, and no meningeal signs were noted. Pertinent laboratory findings were as follows: Hb 8 g/dl, RBC 238 x 10(4)/microliter, WBC 2,900/microliter (band 1.0%, seg 18.5%, lym 28.0%, mono 44.0%, Baso 2.5%), Plt 13 x 10(4)/microliter, PT 16.6"/10.9", APTT 44.7"/35.0". CSF contained 87 mg/dl of protein, 155 mg/dl of glucose and 2 mononuclear cells/microliter. Bone marrow was slightly hypercellular with mild increase in blast forms. No chromosome abnormality was found. CT and MRI revealed a large mass in the left fronto-parietal region and the meninges showed marked thickening with enhancement after gadolinium-DTPA in MRI. The patient was treated with glycerol and steroid, but the subsequent course was complicated by a seizure, agitation, and pneumonia. He died from respiratory failure on January 13, 1996. The patient was discussed in a neurologic CPC and the chief discussant arrived at the conclusion that the patient had chronic myelomonocytic leukemia with infiltration of leukemic cells into meninges and the parenchyme of the cerebrum. Thickening of the dura was thought to be in part a reaction to the subdural hematoma as well as to leukemic cells along the meninges. Postmortem examination revealed hypercellular bone marrow with increase in monocytic cells (more than 20%). The lungs showed pneumonia with scattered old tuberculous lesions. The heart showed an old myocardial infarction in the posterior wall of the left ventricle. The brain showed an old chronic subdural hematoma in the left fronto-temporal region and a cystic mass lesion in the left frontoparietal region. The mass was hypercellular and most of them were monocytes. The dura mater showed reactive thickening without leukemic cell infiltration. It was concluded that this patient had chronic myelomonocytic leukemia with a formation of leukemic mass in the brain. Pathologists thought that the mass was a hematogenous spread. It is rare for chronic myelomonocytic leukemia to form a mass lesion in the brain.
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PMID:[A 45-year-old man with peripheral monocytosis and right hemiparesis]. 962 75


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