Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0018681 (headache)
 56,091 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We report a 57-year-old woman with progressive gait disturbance, headache, character change, convulsion and coma. She was well until 55 years of age, when she noted an onset of unsteady gait. At times she experienced transient weakness in her right hand, which was followed some difficulty in articulation. She was admitted to our service for the work up on April 6, 1992. Neurologic examination at that time revealed an alert Japanese lady in no acute distress. She was oriented to all spheres, however, she was somewhat bradyphrenic and had some disturbance in recent memory. Higher cerebral functions appeared intact. The visual acuity and visual fields were normal as were the optic fundi. Pupils were round and isocoric reacting promptly to light. Ocular movement was full, however, horizontal nystagmus was noted upon right lateral gaze. The sensation of the face was intact. She showed right facial paresis of the central type. Hearing was intact. She showed slurred speech and some difficulty in swallowing. The tongue was deviated to the right. Her gait was wide based and unsteady; tandem gait was difficult, however, walking on toes and on heels were performed well. No cerebellar ataxia was noted, but she showed some clumsiness in her right hand. Deep reflexes were symmetric and normally reactive; plantar response was extensor bilaterally. Sensation was intact; no meningeal sign was elicited. Routine laboratory work up was unremarkable; the CSF was under a borderline pressure (180 mmH2O) and contained 39 mg/dl of protein and 59 mg/dl of sugar. Cranial CT scan revealed diffuse low density areas involving bilateral cerebral white matter as well as the brain stem; MRI revealed high signal intensity lesions in those areas; gadolinium enhancement was negative; cortical sulci were effaced and the anterior part of the left lateral ventricle was compressed without deviation of the midline structure. The patient was treated with steroid pulse therapy without effect. She was discharged for out patient follow up, however, she developed a convulsion which was followed by loss of consciousness, and was admitted again to our service. She had never gained consciousness after this episode, and remained in the state of akinetic mutism. Follow-up CT and MRI did not show much change, although the area of high signal density lesions slightly enlarged on June 1, 1993. Her clinical course was complicated by drug induced bone marrow suppression and nephrotic syndrome. She expired on September 8, 1993 after developing sudden drop of blood pressure and bradycardia.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:[A 57-year-old woman with gait disturbance, headache, character change, convulsion, and coma]. 761 89

A 37-year-old woman with complaints of headache and nausea presented with temporary disturbance of consciousness, bulbar palsy and ataxic speech following flu-like symptoms. After the recovery of her consciousness, she developed orthostatic syncope and numbness all over the body. When she was admitted to our hospital two months later, she showed emaciation, diminished sweat production and butterfly-patch-like pigmentation. Neurologic examinations were remarkable for anisocoric pupils that sluggishly reacted to light, impaired left facial movements, bulbar palsy, numbness of the whole body, total loss of all tendon reflexes, incordination, ataxic gait and severe postural hypotension. Laboratory data included albuminocytogenic dissociation in cerebrospinal fluid, convergence nystagmus and dysmetria in electronystagmography, and right trigeminal paralysis in blink reflex. A sural nerve biopsy showed active axonal degeneration and severe loss of both myelinated and unmyelinated fibers. Examinations of autonomic nervous system disclosed diffuse impairment of sympathetic and parasympathetic postganglionic nerve. Based on these findings she was diagnosed as having acute pandysautonomia. High titer of serum EB virus antibody suggested that acute pandysautonomia and diffuse brainstem impairment may be related to EB virus infection.
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PMID:[A case of acute pandysautonomia and diffuse brain stem impairment associated with EB virus infection]. 772 95

Two Williams syndrome patients are presented who had neurologic symptoms secondary to Chiari malformation type I. Both patients had many of the well-known medical problems found in Williams syndrome. In addition, Patient 1 developed headache, diplopia, and tinnitus at 26 years of age. Neurologic examination revealed intermittent nystagmus and brisk reflexes. Magnetic resonance imaging demonstrated Chiari malformation type I; neurologic symptoms abated following surgery. Patient 2 had a normal neurologic examination at 2 years of age except for hyperreflexia and tight heel cords. At age 10 years, she had generalized contractures, decreased strength and wasting of hand musculature, and hyperreflexia. Magnetic resonance imaging documented Chiari malformation type I. Both patients have significant dysphagia and fusion of cervical spine segments noted on radiography. Morphometric analyses of intracranial contents based on midsagittal magnetic resonance images were performed. This analysis suggests that, compared to age-matched controls, the posterior fossa size is selectively diminished in Williams syndrome, whereas the cerebellum is normal in size. This "mismatch" between the size of the posterior fossa bony compartment and its neural contents may place Williams syndrome patients at high risk for developing Chiari malformation type I.
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PMID:Association of Chiari I malformation and Williams syndrome. 774 69

A 66-year-old man suddenly developed bilateral ptosis after awaking from a nap. He did not experience nausea, vomiting or headache. In the emergency room, high blood pressure was noted. On examination, his consciousness was clear. Ptosis was present bilaterally and worse on the right side. The pupils promptly constricted to light. He could fully adduct his eyes during conjugate gaze movements, but convergence was impaired in the right eye. There was no diplopia or nystagmus. The assessment of the motor and sensory systems revealed no significant findings. Computed tomographic scanning and magnetic resonance imaging of the brain showed a small hematoma in the midbrain. Six months later, ptosis improved; however, the convergence deficit remained.
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PMID:Midbrain hemorrhage presenting as bilateral ptosis without hemiplegia: a case report. 775 61

We report a 65-year-old woman with progressive multiple cranial neuropathy. She had been suffered from bronchial asthma since 1979 for which prednisolone had been prescribed. She noted an onset of pain around her nose in October, 1989, which extended into the periorbital regions bilaterally. In February, 1990, she was treated with stellate ganglion block and trigeminal nerve block; these treatments partially alleviated her pain. In May of 1991, she noted a difficulty in swallowing solid foods. In November of the same year, she developed right facial paresis; two weeks later, she noted numbness in her left face, and was hospitalized to our service on December 16, 1991. On admission, she was afebrile and general physical examination was unremarkable except for piping rales in her both lung fields. On neurologic examination, she was alert and oriented to all spheres; higher cerebral functions were intact. In the cranial nerves, her olfactory sense was lost bilaterally; her vision was markedly diminished bilaterally only to recognize hand movements; the optic fundi appeared normal; the pupils were isocoric and reacted to light promptly. The extraocular muscles were moderately weak to most of the directions more on the left; no nystagmus was present. Facial sensation was diminished bilaterally; the jaw deviated to right; right facial paresis of peripheral type was present; her hearing was diminished bilaterally more on the right. The movement of the soft palate was diminished on the right side; dysphagia was present; her voice was horse; the gag reflex was diminished. The sternocleidomastoid muscle was weak bilaterally; the tongue appeared normal. Examination of gait was differed because of headache, however, no apparent motor weakness was present. No ataxia or involuntary movement was noted. Deep reflexes were normally elicited and symmetric. Plantar response was flexor. Sensation in the extremities was intact. Kernig's sign was positive at 70 degree leg extension; eyeball tenderness was also present bilaterally, however, no nuchal stiffness was noted. Following abnormalities were present in the laboratory examination: WBC 11,400/microliters, ESR 50 mm/hr, CRP 6.1 mg/dl. The lumbar CSF was under a normal pressure containing 29 WBC/microliters (neutrophils 7, lymphocytes 20, others 2), 67 mg/dl of protein, and 53 mg/dl of sugar; cultures for acid-fast bacilli as well as for other bacteria were negative; no malignant cells were found. A cranial CT scan revealed an isodensity mass in the orbit and ill-defined low density areas in the white matters of the frontal lobes.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:[A 65-year-old woman with headache, facial pain, and progressive multiple cranial neuropathy]. 787 85

We report a 50-year-old male having metamorphopsia associated with retinal edema. He was well until one month prior to the present admission when he developed occipital headache and backache. Three weeks later, he noted a sudden onset of twisting of visual images. On admission, he was in no acute distress with well preserved general conditions. Only neurological abnormalities were bilateral papilledema, retinal edema and horizontal nystagmus with a rotatory component. Routine blood chemistries were unremarkable. The CSF contained 28 cells/cmm with 60% consisting of large atypical cells. Cranial CT scans revealed no mass, however, the magnified orbital CT showed bilateral swelling of the optic nerve. He was treated with ventriculoperitoneal shunt and Ommaya tube placement through which methotrexate, cytarabine and prednisolone were administered. He was also treated with systemic cisplatin, mitomycin-C and 5-fluorouracil. With these therapy, his headache, metamorphopsia and papilledema improved. He was discharged for out-patient follow-up, however, he had to admitted again because of progressive difficulty of gait and loss of appetite. On admission, he complained of severe backache, and his gait disturbance appeared to be in part due to his backache. A slight weakness was noted in all four limbs with loss of deep reflexes. Mentally he was alert and cranial nerves appeared intact without papilledema. But nuchal rigidity was noted. Cranial CT scan revealed attenuation of all the cortical sulci and marked diffuse low density changes in the cerebral white matter, and his chest film revealed a ring-shape shadow in his left lung field. He deteriorated progressively with terminal gastrointestinal hemorrhage. He expired three weeks after his second admission.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[A 50-year-old man with metamorphopsia and optic nerve swelling]. 819 34

A 13-year-old boy complained of frequent headaches and diplopia on rightward gaze. A CT scan demonstrated hydrocephalus and a non-homogeneous enhancing mass in the pineal area, leading to a diagnosis of pineal tumor. The physical examination revealed no abnormalities. On neurological examination, there were a right homonymous hemianopsia and slight choked disc in both optic fundi. His right eye was slightly adducted on primary gaze. On right lateral gaze, his right eye could not move beyond the midline and showed gaze paretic nystagmus, whereas his left eye could move fully in all directions. The abducens palsy could be overcome by the oculocephalic maneuver or caloric test. Interestingly, his right eye could abduct when his left eye was covered. From these finding, this was labelled a supranuclear abducens palsy. The convergent nystagmus was observed. Rightward OKN (quick phase to right) of the right eye was abolished with and without the left eye covered, while leftward OKN of the right eye was preserved. Pursuit to right was disturbed. After removal of the tumor, the gaze palsies disappeared. It is postulated that the supranuclear lateral gaze palsy was caused by impairment of supranuclear control by involvement of lateral gaze pathways to gaze center coursing near the oculomotor nucleus.
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PMID:[Unilateral supranuclear abducens palsy in a pineal tumor]. 819 45

In this paper we present a case of glioma which was located in the cerebellopontine angle. The patient, a 3-year-old male, experienced difficulty with gait for one month before admission. He was admitted to Toyota Memorial Hospital on February 2, 1991, suffering from severe headache and vomiting. Neurological examination upon admission revealed horizontal nystagmus and ataxia. MRI revealed a mass in the cerebellopontine angle. Craniotomy was performed on February 4, 1991, and a tumor was revealed in the cerebellopontine angle. The tumor was clearly demarcated and encapsulated; the cerebellum and brainstem were compressed without damage. Most of the tumor was removed. A histopathological summary of the tumor follows. The tumor appeared as exophytic lesions on the pons, extending into the cerebellopontine angle. Tumor cells contained small round nuclei and acidophilic cytoplasm. The oncocyte, which was growing endomorphically, revealed a short-cell projection, suggesting a tendency to penetrate blood vessels. Intercellular microcystic degeneration was observed clearly, with some parts of the oncocyte forming a myxoid matrix. Immunohistochemically, most of the tumor cells reacted positively to Vimentin, but negatively to S-100 protein and GFAP. Given the pathological information, the tumor was interpreted as anaplastic astrocytoma. Postoperative radiation therapy was performed, but the patient died four months later because the tumor had spread to the brainstem. In this paper we discuss the differential diagnosis of the cerebellopontine angle tumor and the appearance of anaplastic astrocytoma as exophytic lesions on the pons and the spread of the tumor into the cerebellopontine angle.
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PMID:Anaplastic astrocytoma in the cerebellopontine angle. 822 Jul 82

We present a female patient with typical third stage neuroborreliosis with progressive chronic encephalomyelitis. One month after a tick bite, in the first stage of Lyme disease, she had myalgias during ten days and after one year polyarthralgias and polyarthritis. Neurological problems occurred 15 years after the tick bite with headache, nystagmus, intentional tremor and spastic paraparesis with sphincter disturbances. Etiological diagnosis was established after three years. Cytobiochemical findings in cerebrospinal liquor were normal but oligoclonal IgG bands were found. Fluorescent antibody test was positive in serum (1:75) as well as ELISA (1:447). The patient reacted favourably to intravenous crystal penicillin 20 x 10(6) units daily during 18 days. Till now, she is in remission and has only mild paresis of the left leg.
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PMID:[Chronic encephalomyelitis caused by Borrelia burgdorferi. Case report]. 826 11

A 55-year-old man first noted a swelling on his back in September 1990, when CT scan of his chest suggested a pleural fistula and a cold abscess. In the following month, he became pyrexial and felt nauseated with headache. Subsequently he was transferred to our hospital. Results of neurological examination were abnormal only in that he had neck stiffness and bilateral nystagmus with drowsiness. Cerebrospinal fluid (CSF) showed turbid yellowish fluid with an opening pressure of 360 mmH2O, a protein content of 173 mg/dl, a glucose level of 19 mg/dl, and a white blood cell count of 3,024/ml (75% polymorphs, 25% lymphocytes). Tryptophane test was positive. No bacteria, fungi or acid-fast bacilli were seen on direct smear. Adenosine deaminase activity in CSF was 13.9 IU/l. Antibiotics, antituberculous drugs, corticosteroids and glycerol were administered. The clinical course in the hospital was satisfactory for the next two months, but a contrast enhanced CT scan showed prominent enhancement in the left choroid plexus, and MRI revealed another mass in the subarachnoidal space under the right frontal lobe. An open biopsy was done on the massive lesion in the frontal lobe. Macroscopically, this lesion was an encapsulated granulomatous one. On the other hand, there were groups of epitheloid cells with micronecrosis in their centers microscopically. These findings were compatible with tuberculoma, in spite of the absence of acid-fast bacilli or caseous necrosis. Medication was intensively continued: a follow-up CT showed gradual reduction of the choroid plexus lesion and shrinkage of the left lateral ventricle.
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PMID:[A case of tuberculous meningitis with abnormal contrast enhancement of choroid plexus on CT and MRI]. 829 13


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