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

We reported a case of simultaneous medullary hemorrhage and hematomyelia. A 93-year-old woman, who had hypertension, was admitted to our hospital because of headache, numbness and weakness of the left extremities, and somnolence. On admission, weakness and disturbance of tactile sensations were observed in the left extremities. Magnetic resonance imaging showed medullary hemorrhage and hematomyelia and these two lesions were separated. Medullary hemorrhage was at the left dorsal paramedian area within mid-lower medulla oblongata, and hematomyelia was at the left side of the gray matter from medullo-cervical junction to upper cervical cord. Five days later from admission, weakness occurred in the right lower extremity and also in the upper extremity. This process suggested that the main lesion of tetraparesis was medullo-cervical junction. Review of 16 cases of medullary hemorrhage demonstrated that frequent neurological signs were palatal weakness, nystagmus, and disturbance of pain and temperature sense. But our case showed only disturbance of tactile sensations. Review of 19 cases of hematomyelia demonstrated that frequent neurological signs were sensory disturbance, paralysis and localized pain. Our case showed only paralysis. The cause of simultaneous hemorrhage was considered arteriovenous malformation or simultaneous multiple hypertensive hemorrhages.
 ...
PMID:[A case of simultaneous medullary hemorrhage and hematomyelia]. 1065 65

A 40-year-old normotensive man suddenly developed diplopia, tinnitus and a burning sensation on the left side of his body while driving a motorcycle. He did not complain of headache, nausea or vomiting. Neurologic examination revealed left trochlear nerve palsy and impaired pinprick, temperature and joint position sensation of the left limbs. There was no ptosis or motor deficit. He had a mild bleeding diathesis due to alcoholic liver cirrhosis. Computerized tomography and magnetic resonance image of the brain disclosed hemorrhages in the right midbrain tectum and the left temporal lobe. After nine months of observation, there was nearly complete recovery of symptoms, except for mild residual diplopia. From a literature review, only nine case of midbrain tectal hemorrhage involving the inferior colliculus have been reported. These patients had a unique clinical presentation. Diplopia due to trochlear nerve palsy, either unilateral or bilateral, was present in all of the cases. Tinnitus and sensory disturbance contralateral to the lesion side were very common. Only three patients had risk factors for hemorrhage, including bleeding diathesis, hypertension and vascular anomalies. In the majority of patients, no underlying causes were detected. The outcome was favorable with conservative treatment.
 ...
PMID:Midbrain hemorrhage presenting with trochlear nerve palsy. 1067 25

We experienced a patient of CIDP who was twice complicated with aseptic meningitis following high-dose intravenous gammaglobulin therapy. The patient was a 29-year-old woman who first developed gait disturbance in September 1998. Neurological examination revealed muscle weakness and sensory disturbance in the distal parts of four extremities and decrease of deep tendon reflexes. Cerebrospinal fluid analysis revealed an elevated protein content and a normal cell count. Steroid therapy was effective in early stage, however, this effectiveness had been reduced gradually. She received high-dose intravenous gammaglobulin administrations in September 1999. On the fourth day after start of this therapy, she developed severe headache, nausea and nuchal rigidity without fever. Cerebrospinal fluid analysis revealed an increased cell count of mononuclear predominance and an elevated protein content. As bacterial culture remained negative and viral titers were not elevated, aseptic meningitis was diagnosed. The therapy was stopped, and thereafter her headache continued for 7 days. The muscle weakness and sensory disturbance were remarkably improved, but 9 months later, her symptoms became worse again. She received high-dose gammaglobulin administrations for 2 days in June 2000 and developed aseptic meningitis again. Over again, 9 months later, she received the same medication for only 1 day in March 2001 and she developed mild headache but not meningitis. Aseptic meningitis with CIDP following high-dose gammaglobulin therapy was rare, however, we should pay attention to this therapy in patients with CIDP and may prevent the occurrence of aseptic meningitis by reducing the total dose and shortening the administration periods of gammaglobulin.
 ...
PMID:[A case of recurrent aseptic meningitis caused by high-dose intravenous gammaglobulin therapy for chronic inflammatory demyelinating polyneuropathy]. 1208 Jun 12

We report 9 patients (5 males, 4 females, ages 63-77) with chronic polyneuropathy. They were exposed to arsenic for about 15-40 years in Toroku Valley, Takachiho-Town, Miyazaki Prefecture, Japan, where a mining company produced arsenic from 1920-1962. Predominantly sensory polyneuropathy was the most significant neurological finding. In 5 of them, superficial and deep sensation was equally affected over the entire body, including head, face, and mucous membranes of the mouth. The corneal reflexes were absent or sluggish. Pin-prick and light-touch perception was absent in their hands and legs. Another sensory disorder such as glove and stocking-type was seen in 4 of them. All 9 patients were comfortable with extremely hot water in their beverages, their baths, and their wash basins compared with controls. But these patients felt that their temperature sensation was normal. Motor involvement was minimal. Although motor-nerve conduction velocities were normal or reduced minimally, sensory-nerve conduction velocities were moderately reduced. Sural-nerve biopsy revealed reduction of both small myelinated and unmyelinated fibers, which occurs with axonal degeneration of peripheral nerves. Other main symptoms and signs were tension-type headaches, non-painful tonic spasms of limbs, and losses or significantly decreased sensations of taste and smell. Dantrolene-sodium was effective for the treatment of their non-painful tonic spasms of limbs. As for the general medical condition of these patients, all of them had suffered from chronic bronchitis and skin eruption during childhood or in their early life or in their young adulthood when the mine was producing arsenic. At the time of this study only four of them suffered from chronic bronchitis and none of them had skin eruptions or discoloration of the skin, 37 years after closure of the mine. These 9 patients were diagnosed as having chronic arsenic poisoning and arsenic polyneuropathy. The multiplicity of symptoms found in these patients--anosmia, ageusia, chronic bronchitis, tension-type headaches, and non-painful tonic spasms of limbs--differs from the symptoms previously reported cases with arsenic poisoning. This may be due to combined overexposure to environmentally hazardous arsenic by effluent gas, dust, and drinking water in Toroku Valley. As concerns the sensory disorders described above, it is necessary to investigate sensory conduction pathways, including cerebral sensory cortex, spinal cord, and skin sensory receptors such as Pacini corpuscles, and Meissner corpuscles. Unfortunately, no information has been obtained about this problem because there were no autopsy cases.
 ...
PMID:[Chronic and predominantly sensory polyneuropathy in Toroku Valley where a mining company produced arsenic]. 1260 76

A 42-year-old man complained of severe left orbital pain for 7 months. The diagnosis of cluster headache was made on the basis of diagnostic criteria formed by the International Headache Society. Sumatriptan was effective in relieving pain to a certain degree, but the frequency of the occurrence of pain gradually increased. Subsequently, he presented sensory disturbances in the left trigeminal nerve, and was admitted to our hospital. On admission, his neurological examination revealed left miosis and paresthesia in the first branch of the left trigeminal nerve. Neither anhidrosis nor ptosis was noted. His autonomic failure was consistent with post-synaptic disturbance as determined by pharmacological analysis for pupil's function. On the basis of the unique combination of neurological sings and symptoms including the unilateral headache, partial Horner's syndrome, and V1 sensory disturbance, we diagnosed him as having Raeder's syndrome. To exclude the possibility of a lesion in the Gasser ganglion of the middle fossa of the cranium or carotid artery causing symptomatic Raeder's syndrome, imaging studies including brain MRI, cervical MRA, and Doppler ultrasonography were performed, which revealed normal findings. We started him on oral prednisolone at 1 mg/kg once a day, which resulted in a rapid and dramatic suppression of pain. Thus, this case showed a progression from cluster headache to idiopathic Raeder's syndrome, which suggests that these two disorders might share common pathological and anatomical lesions.
 ...
PMID:[Progression of cluster headache to Raeder's syndrome with marked response to corticosteroid therapy: a case report]. 1591 3

The patient was a 29-year-old man with sinusitis. He was admitted with high grade fever, headache, vomiting and disturbance of consciousness. Neurological examination revealed nuchal rigidity, aphasia, right hemiparesis, right sensory disturbance and bilateral Babinski signs. A nonenhanced CT on admission showed a low density area in the interhemispheric fissure. Gadolinium-enhanced MRI and DWI showed an interhemispheric subdural empyema and sinusitis. Neurological deficits gradually improved, after he underwent urgent surgical drainage of sinusitis followed by antibiotics therapy. About three weeks later, he developed right hemiparesis and disturbance of consciousness, and MRI demonstrated the expansion of interhemispheric subdural empyema. Therefore, he underwent surgical drainage of interhemispheric subdural empyema. He was discharged from our hospital without neurologic deficit. We suggest that MRI, in particular DWI, is a useful additional imaging modality for the diagnosis of interhemispheric subdural empyema.
 ...
PMID:[A case of interhemispheric subdural empyema with sinusitis diagnosed by diffusion-weighted MRI]. 1602 72

Trigeminal neuropathy is characterized by sensory disturbance of the division of trigeminal nerve, and sometimes is associated with pain. Trigeminal neuropathy secondary to perineural invasion of sinonasal lymphoma is extremely rare. Likewise, sinonasal lymphoma is infrequently demonstrated initially with cranial neuropathy. The present case served to broaden the differential diagnosis of secondary trigeminal neuropathy and to alert clinicians to cautiously assess perineural spread of occult neoplasm in sinonasal tract and larynx or pharynx for cases with evolving trigeminal neuropathy or even other cranial nerve neuropathy in which no definite cause is identified.
Headache 2007 Feb
PMID:Perineural invasion of sinonasal lymphoma: a rare cause of trigeminal neuropathy. 1730 Mar 75

We report a case of multiple gangliogliomas of the optic pathway in an 18-year-old boy. He presented with visual disturbance mainly in his left eye, non-specific headaches, and episodes of sensory disturbance in his left arm. Visual acuity was 6/9 and 6/24 in his right and left eye respectively. He did not have any Lisch nodules. Optic atrophy was noted in his left eye. MRI scan revealed multiple enhancing lesions involving the optic chiasm, left optic tract, right lateral geniculate body, and right optic radiation in the temporal lobe. Stereotactic biopsy of the temporal tumour confirmed ganglioglioma. Multiple gangliogliomas of the optic pathway has not been hitherto described.
 ...
PMID:Multiple gangliogliomas of the optic pathway. 1743 99

A 57-year-old woman who had severe opticospinal multiple sclerosis (OSMS) was admitted to our hospital. She had presented with visual loss and gait disturbance at the age of 48, and had since experienced more than 10 relapses and been hospitalized 9 times. Interferon beta-lb treatment (8,000,000 units on alternate days) had been started at her last admission. Prior to the present admission, she had developed left visual loss and gait difficulty after headache lasting a few days. Cerebrospinal fluid showed elevation of cell count (322/mm3), protein (130 mg/dl), and myelin basic protein (462 pg/ml; normal, <102 pg/ml). On examination, she exhibited decreased left visual acuity, paraplegia, ataxia of the right upper extremity, and sensory disturbance, particularly in the lower extremities. Bowel and bladder disturbances were also evident Laboratory testing showed lymphocytopenia (420/microl), compared to a white cell count of 1700/microl just before initiation of interferon beta-lb1therapy. MRI revealed a new lesion in the cerebellum in addition to small T2-hyperintense lesions in the white matter of the brain;these had been noted previously. Interferon beta-1b therapy was ceased and she was treated using methylprednisolone pulse therapy. After the abnormal findings resolved, however, interferon beta-lb1therapy was restarted. Three months after, she exhibited right hemiparesis without facial palsy concurrent with lymphocytopenia. MRI showed T2-hyperintense lesions in the periventricular white matter, left cerebral peduncle, bilateral middle cerebellar peduncles, and right cerebellar hemisphere. We reduced the doses of interferon beta-lb1immediately. Thereafter, she did not have relapse for 29 months, but her EDSS (expanded disability status scale) has not recovered. Although interferon beta-lb1has been recognized as an effective drug for decreasing the relapse rate and severity of both secondary progressive MS and relapsing-remitting MS, the present case showed the possibility of interferon beta-1b being associated with phenotype change from OSMS to conventional MS (CMS).
 ...
PMID:[Case of opticospinal multiple sclerosis showing phenotype change to conventional type induced by interferon beta-1b]. 1751 Dec 77

A 17-year-old boy with high fever, headache, and neck stiffness was admitted to our hospital. Spinal fluid showed a protein level of 215 mg/dL with myelin basic protein (579 pg/mL), 347/ microl cells (330 mononuclear cells), and a glucose level of 53 mg/dL. One week later, urinary retention, flaccid paraplegia, and sensory disturbance below the 10th thoracic level developed. MRI of the spinal cord revealed swelling and T2-high intensity area in the cord at the 11th and 12th thoracic level. Although high-dose of methylprednisolone was administered, consciousness disturbance and respiratory failure that required mechanical ventilation occurred. Bilateral abducens nerve palsy, nystagmus, and flaccid tetraparesis also occurred. Brain MRI revealed T2-high intensity area in the midbrain and pons. Nerve conduction study showed diminished amplitudes and prolonged latencies or absence of F waves. The patient was administered a combination of intravenous immunoglobulin and a high-dose of methylprednisolone. He showed improvement within one week after the treatment. Two weeks later, he recovered from respiratory failure and weakness of the upper limbs. He remained paraplegic, but gradually improved and was able to walk with support one and a half years later. We suggest the combination therapy of intravenous immunoglobulin and a high-dose of methylprednisolone is effective for patients with combined ADEM and peripheral neuropathy.
 ...
PMID:[A case of acute disseminated encephalomyelitis (ADEM) associated with peripheral neuropathy]. 1751 Dec 89


<< Previous 1 2 3 4 5 6 Next >>