Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0040822 (tremor)
 18,428 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Dementia, a syndrome of acquired intellectual deterioration, is an etiologically nonspecific condition that can be permanent or reversible. When evaluating demented patients, a careful exposure history will determine the possible role of drugs, metals, or toxins. Physical examination may reveal focal deficits in cases of intracranial mass lesions and spasticity or ataxia of the lower limbs if hydrocephalus is present. Coexistence of dementia and a peripheral neuropathy usually indicates the existence of a toxic or metabolic disorder. Depressed mood, sleep disturbance, anorexia, impotence, constipation, and psychomotor retardation indicate the presence of a depressive syndrome. Asterixis, myoclonus, and postural tremor are common in toxic-metabolic dementias, whereas resting tremor, choreoathetosis, or rigidity occur in progressive extrapyramidal disorder. EEG is focally abnormal in cases of cerebral mass lesions and shows generalized slowing in toxic-metabolic encephalopathies. CT will aid in the identification of hydrocephalus, subdural hematomas, and intracranial mass lesions. A thorough laboratory evaluation including complete blood count, erythrocyte sedimentation rate, electrolytes, blood urea nitrogen and blood sugar, liver and thyroid function tests, serum calcium and phosphorus levels, B12 and folate levels, serum copper and ceruloplasmin, VDRL, chest X-ray, electrocardiogram, and lumbar puncture may demonstrate treatable disorders that are adversely affecting intellectual function. Elderly individuals are particularly susceptible to the effects of toxic or metabolic disorders, and a mild dementia may be exaggerated by relatively minor fluctuations in metabolic status. Treatable causes of dementia should be sought in all demented patients.
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PMID:Treatable dementias. 635 58

Pneumoencephalography was performed in 35 patients with a significant diagnosis of disseminated sclerosis. Enlargement of the III ventricle was revealed in 21 patients (60%), dropsy of lateral ventricles in 16 (45,6%) and that of the IV ventricle in 13 (37,2%), atrophy of brain stem in 9 (25,4%), block of the subarachnoidal space in 11 patients (31,4%). The most pronounced brain changes were seen in patients with a cerebellar form of disseminated sclerosis and in those having severe motor disturbances, ataxia and tremor. The degree of hydrocephalus did not depend on the disease duration. A possible pathogenetic role of dropsy in disseminated sclerosis is discussed. Hydrocephalus may be considered as an additional clinicoroentgenological feature of disseminated sclerosis.
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PMID:[Pneumoencephalography in multiple sclerosis]. 671 Dec 3

A 28-year old male was admitted to Musashino Red Cross Hospital on June 21, 1975, because of symptoms of increased intracranial pressure and cerebellar dysfunction. Thirteen months prior to admission he had a mild fever, tremor of right arm, headache, nausea and unsteady gait, but made a gradual recovery in about 40 days. A month prior to admission he had unsteady gate again wit dizziness, photophobia and lacrimation. Gait disturbance aggravated and he was admitted to another hospital, where he developed recent memory disturbance and cloudiness of consciousness. Spinal tap revealed initial pressure of 280 mm CSF. So a mass lesion possibly in the posterior fossa was suspected and the patient was referred to the neurosurgical department of musashino Red Cross Hospital. On admission he was moderately disorientated and disturbed in recent memory. Wide based gait, horizontal and vertical nystagmus were also noted. Angiography revealed rounding of the curve of the pericallosal artery but no space occupying lesions. External ventricular drainage was performed on July 25, 1975. After the operation, his orientation improved without change in dizziness, nystagmus and recent memory disturbance. Ventriculography showed hydrocephalus with cisternography revealed a block at the basal cisterns. PPDs was negative and typical sarcoid tubercles were found in the biopsy specimen of the cervical lymphnode. Kveim test was positive. But repeated chest roentgenogram failed to show bilateral hilar lymphadenopathy, or other changes consistent with pulmonary sarcoidosis. Steroid therapy resulted in marked symptomatic improvement.
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PMID:[A case of CNS sarcoidosis -case report of hydrocephalus due to mechanical obstruction secondary to sarcoid granulomata at the outlet of the fourth ventricle (author's transl)]. 723 30

Spinal cavernous hemangioma is rare, and it is extremely rare for cavernous hemangioma to develop in the cauda equina. There has been only one report of hydrocephalus associated with cavernous hemangioma in the cauda equina. We report a case of cavernous hemangioma in the cauda equina diagnosed on the basis of the headaches due to hydrocephalus. A 67-year-old man was being treated for Parkinson's disease because of tremor of both upper extremities for several years. In December 1991 he complained of occasional headaches. On February 15, 1992 the headaches became severe and frequent, with nausea and vomiting, and his gait became unsteady. Four days later he came to our hospital. Neurological examination revealed fine finger tremor and truncal ataxia. Computerized tomography scanning and magnetic resonance imaging of the head revealed ventricular enlargement, but there were no mass lesions obstructing the cerebrospinal fluid pathway. Lumbar puncture at the L3-L4 level yielded bloody cerebrospinal fluid, and the pressure had increased to 410 mmH2O. Cerebral angiography showed no abnormal findings. Magnetic resonance imaging of the lumbar spine demonstrated an intradural tumor at the level of vertebral body L2. Spinal angiography showed no evidence of abnormal vascularity in the mass at the L2 level. On March 10, 1992, laminectomy at three levels, L1 to L3 was performed, and a well-defined blueberry-like intra-cauda equina tumor 1 cm. in diameter, was removed. One spinal nerve root passed through the tumor. The pathological diagnosis was cavernous hemangioma. After removal of the tumor, the patient's headaches improved, and a follow-up computerized tomography scan six months later showed normal ventricle size.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Cauda equina cavernous hemangioma associated with hydrocephalus--case report]. 754 25

Parkinsonism is an uncommon movement disorder in childhood. Six unusual cases of acquired parkinsonism in hospitalized children are described. Clinical manifestations included an akinetic-rigid syndrome with and without tremor, the combination of parkinsonism and dystonia, and a parkinsonism-plus syndrome. Altered mental status, mutism, dysphagia, and sialorrhea were frequent associations. Etiologies included hypoxic-ischemic encephalopathy; haloperidol treatment with and without neuroleptic malignant syndrome; toxicity of cytosine arabinoside, cyclophosphamide, amphotericin B, and methotrexate; St. Louis encephalitis and other encephalitides; and a pineal tumor with hydrocephalus. Cranial magnetic resonance imaging results ranged from normal to profound cerebral and cerebellar atrophy with chemotherapeutic toxicity. The illnesses usually were severe enough to require pharmacotherapy. Incorrect diagnoses of depression or catatonia delayed treatment or aggravated the problem. Acute treatment included amantadine, levodopa/carbidopa with or without selegiline, diphenhydramine, or benztropine. The concentration of CSF homovanillic acid was normal in a neuroleptic-associated patient, but the level was low in an encephalitic patient. All patients demonstrated dramatic improvement, including two who were not treated; some had complete resolution of symptoms and none required continued antiparkinsonian drugs despite poor scores on the Unified Parkinson's Disease Rating Scale and the Modified Hoehn and Yahr Rating Scales. The causes of parkinsonism described are more common in a general pediatric hospital than the parkinsonism associated with the popularized Segawa syndrome.
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PMID:Clinical spectrum of secondary parkinsonism in childhood: a reversible disorder. 802 61

Freezing gait is an incapacitating symptom often observed in patients with Parkinson's disease. It has been less frequently described in association with multi-infarct state, multisystem atrophies, and normotensive hydrocephalus. In our movement disorder clinic, we have diagnosed (and followed up to 3 years; median, 16 months), 18 patients in whom progressive freezing gait was the sole neurological dysfunction. These 15 men and 3 women (aged 60-82 years; 74 +/- 6) were subjected to an extensive neurological workup that included clinical evaluation, videotaping for grading of gait disability, comprehensive blood and cerebrospinal fluid (CSF) analysis, and brain computed tomography (CT) and magnetic resonance imaging (MRI). Mean disease duration was 2.5 +/- 1.9 years (range, 0.5-6). Neurological examination disclosed freezing gait, often associated with varying degrees of postural instability. The degree of freezing gait ranged from sudden motor blocks only when confronted with obstacles to severe disability with total inability to start walking requiring a walker, massive assistance, or a wheelchair. However, patients could mimic gait movements with absolutely no freezing when seated or lying prone, and most of them could overcome arrests by the "walking-over-lines" maneuver. Otherwise, neurological examination was normal with no signs of bradykinesia, rigidity, or tremor. Blood chemistry and CSF analysis were normal. Brain CT and MRI were normal or showed mild cortical atrophy in 12 and putative lacunes in 6 patients. Therapy with levodopa or dopamine agonists was ineffective. During the follow-up period, a gradual progression of the freezing gait was observed. However, it remained unaccompanied by any other neurological findings.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Primary progressive freezing gait. 834 Dec 93

We report a 32-year-old man who developed cerebellar ataxia and a posterior fossa mass 12 years after the radiation therapy for a cerebellar arteriovenous malformation (AVM). The patient was well until 19 years of the age when he had an acute onset of vertigo and vomiting. A spinal tap was performed and the CSF was bloody. He was admitted to another hospital where an arteriovenous malformation was found in the cerebellum by angiography. Four years after the onset, he developed tingling sensation in the distribution of the second division of the right trigeminal nerve. He was admitted to the neurosurgery service of our hospital where the cerebellar AVM was confirmed. He was transferred to University of California where Bragg peak stereotaxic radiotherapy was successfully performed; this utilizes high energy alpha-ray produced by a cyclotron. Three years after the radiotherapy, marked reduction in the size of the AVM was confirmed by angiography. Twelve years after the onset of his initial symptom, he noted unsteadiness of gait. He was readmitted to our neurosurgery service where obstructive hydrocephalus was found. He was treated by ventriculoperitoneal shunting and placement of a Ommaya reservoir. After these therapy, he noted marked improvement in his gait and ataxia. However, in 1993, his unsteadiness of gait recurred, and he was again admitted to our neurosurgery service on June 20, 1993. On admission, T1-weighted MRI revealed a slightly low signal intensity mass lesion in the right cerebellar hemisphere compressing the brain stem; a spotty high signal intensity lesion and another small low intensity lesion were seen within the mass. Vertebro-basilar angiograms revealed upward displacement of the superior cerebellar arteries. No arteriovenous nidus was visualized. On July, 3rd, the cyst was surgically drained and the Ommaya reservoir was removed. Post-operative course was uneventful, however, he developed head tremor after the surgery. Neurologic examination on July 20, 1993 revealed an alert and well oriented man in no acute distress. General physical examination was unremarkable. Neurologic examination revealed no dementia; higher cerebral functions appeared intact. The optic discs were flat, and visual fields were intact. Ocular movements were full but convergence was restricted. Horizontal gaze nystagmus was noted more in the right lateral gaze. Pupils were intact. Facial sensation and facial muscles were intact. Hearing was normal. His voice was of nasal quality. Pharyngeal reflex was diminished. The tongue showed deviation to the left without atrophy. Head tremor at 5 c/s was noted. He was able to stand with support but was unable to walk. No muscle atrophy or weakness was noted. The finger-to-nose and the heel-to-knee tests showed dysmetria and decomposition more on the right. Rapid alternating movements were ataxic on the right. Muscle tone was diminished on the right. Muscle stretch reflexes were normally elicited and were symmetric. The plantar response was flexor bilaterally. Sensation was intact. On July 21, a posterior fossa exploration was performed. After the surgery, he was treated with 30 mg/day of alotinolol which showed no effect on his head tremor. He was then treated with gradually increasing doses of clonazepam; when he received 8 mg/day of clonazepam, his tremor showed marked improvement. He was discussed in a neurologic CPC on the nature of the posterior fossa lesion and his tremor. Opinions were divided between delayed radiation necrosis and a radiation-induced brain tumor. The chief discussant arrived at the conclusion that the patient had delayed radiation necrosis compressing the brain stem and cerebellar hemispheres. Regarding the nature of his tremor, he thought that his head tremor was of cerebellar type of postural tremor. Histologic examination of the biopsied specimen revealed accumulation of relatively fresh blood constituents in the deep area of the cerebellum forming a mass. Most of the
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PMID:[A 32-year-old man who developed a posterior fossa mass 12 years after the radiation therapy for cerebellar arteriovenous malformation]. 867 25

A 70-year-old female presented with the clinical triad of normal pressure hydrocephalus (NPH) and senile tremor. Neuroimaging disclosed findings of both NPH and empty sella (ES). A ventriculoperitoneal shunt did not modify the clinical course except for a mild and transient improvement, and shunt malfunction occurred later on. The association of NPH and ES may result from a common underlying mechanism such as transient increases in intracranial pressure.
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PMID:Idiopathic normal pressure hydrocephalus associated with empty sella. 958 85

The optimal time for treating congenital hydrocephalus is still unknown. The following study tries to answer this question by shunting hydrocephalic rats around the 10th day of life when the brain development corresponds to that of humans at birth. The animals were allocated to 4 groups: normal, hydrocephalic, normal sham-operated and hydrocephalic-shunted rats (groups 1-4). Body weight and neurological development was tested every 2nd-3rd day. X-rays of the skull were performed in groups 2, 3 and 4 at 10 days and in all at 20 days. In groups 2 and 4 0.1 ml lohexolum was instilled into the lateral ventricle at 10 days and in all at 20 days. X-rays were used to calculate the volume of the neurocranium and to identify ventriculomegaly and its grade (1-3). The x-rays and shunting were performed under general anesthesia, the latter using Kausch's technique. At 20 days of age the animals were sacrificed, the homogenized brain tissue was used to measure Protein, DNA, GAD and CNP by photometry, fluorometry and enzymatically. Time-course of neurological development in group 1: The locomotor patterns were attained gradually up to the ability to hold on to a bar. In group 2 there were larger variations and holding on to a bar was possible only in 6/13. In addition, a distinct tremor was observed in 34%. In group 4 holding on to a bar was possible in all, tremor was observed in 20% of examinations and diminishing following surgery. The volume of the neurocranium in groups 2 and 4 was significantly larger than in groups 3 at 10 days; and in group 2 significantly larger than in groups 1, 3 and 4 at 20 days. In group 4 the ventriculomegaly was distinctly reduced in 7 and remained the same in 1. Protein was significantly lower in group 4. DNA was the same in all groups. GAD was the lowest and the CNP significantly low in group 2. The study shows that an effective shunt may reverse the progressive clinical, radiological and neurochemical changes of hydrocephalus, and that surgery must not be performed necessarily earlier (e.g. prenatally in humans).
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PMID:Clinical, gross morphological and neurochemical follow-up in normal, hydrocephalic and hydrocephalic-shunted rats. 982 33

Two patients are reported in whom the presence of triventricular hydrocephalus and aqueductal obstruction or stenosis due to multiple expanding lacunae in the mesencephalothalamic region possibly corresponds to abnormally dilated perivascular spaces. Placement of a ventriculoperitoneal cerebrospinal fluid (CSF) shunt in one patient and the performance of a third ventricle cisternotomy in the other reversed the hydrocephalic syndrome, but did not modify the complex neuroophthalmological disturbance and rubral tremor presumably related to the compressive effects of the lacunae on adjacent parenchyma. In one patient the number and size of the lacunae were increased 4 years after CSF shunt placement. A review of the literature revealed two cases in which magnetic resonance imaging demonstrated a similar, poorly understood pathological condition.
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PMID:Expanding lacunae causing triventricular hydrocephalus. Report of two cases. 1088 26


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