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Query: UMLS:C0018681 (headache)
 56,091 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Higher cerebral dysfunctions such as aphasia, apraxia and agnosia have seldom been reported in multiple sclerosis (MS). 12 year-old right-handed boy felt unsteadiness of the body and headache for several days. Two months later, he had the same episode and complained of visual disturbance, and weakness and sensory disturbance on the face and the extremities. Additionally, he showed amnestic aphasia, acalculia, ideomotor apraxia, finger agnosia and right-left disorientation. Cerebrospinal fluid examinations revealed increases IgG, myelin basic protein and neuron specific enolase (11%, 25 ng/ml and 28.8 ng/ml, respectively). X-ray CT scan and MRI-CT examinations revealed sclerotic lesions on the left parietal white matter and the right mid-brain. The diagnosis was made as MS. He was treated with m-PSL (methyl-prednisolone) pulse therapy for three weeks and consecutively treated with PSL for four weeks. He recovered gradually, but visual disturbance and facial palsy remained. After seven months MRI-CT showed a high signal intensity on the left parietal white matter in spite of the disappearance of the lesion on X-ray CT scan. We suggest that these higher cerebral dysfunctions may result from the lesion of the left parietal white matter which produces a disconnection between each cortical area.
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PMID:[Multiple sclerosis with higher cerebral dysfunction: a case report]. 199 97

We report a case of intraventricular cystic meningioma in the left lateral ventricle. A-44-year-old male patient was admitted with headache on November 25, 1991. Neurological examination revealed acalculia and left homonymous hemianopsia. CT and MRI showed a solid tumor which originated in the body of the left lateral ventricle, and which was associated with a cystic component postero-laterally. Tumor strains fed by the left anterior choroidal artery and the medial and lateral posterior choroidal artery by angiography. The tumor was totally removed via the lateral temporal parietal approach. Histological examination revealed meningotheliomatous meningioma in the solid tumor and only gliosis in the wall of the cyst.
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PMID:[A case of intraventricular cystic meningioma]. 825 25

The following case report presents a patient exhibiting Gerstmann syndrome accompanied by toe agnosia. A 72 year old right handed woman had a focal lesion in the angular gyrus of the left hemisphere which was caused by a glioblastoma multiforme. The first symptom she had complained of was severe headache. Standardised neuropsychological tests of intelligence, memory, attention, fluency, apraxia, and language functions as well as tests for the assessment of agraphia, acalculia, right-left disorientation, and digit agnosia were performed. The patient displayed all four symptoms of the Gerstmann syndrome--namely, agraphia, acalculia, right-left disorientation, and finger agnosia. The patient did not display aphasia, constructional apraxia, or any other neuropsychological impairment. In addition to the four symptoms of the Gerstmann syndrome an agnosia of the toes was found. Further studies should determine whether finger agnosia in Gerstmann syndrome is usually accompanied by toe agnosia. Finger agnosia in the context of this syndrome may be better named digit agnosia.
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PMID:Toe agnosia in Gerstmann syndrome. 932 65

This case of microsporidiosis manifested as mutiple intracranial lesions separated in space and time, and neurological and radiological findings were improved with albendazole administration. A 33-year-old man presented with headache, fever, and dysphasia. His consciousness was clear. Neurological examination revealed acalculia, agraphia, and homonymous hemianopsia. He had a past history of febrile convulsive seizures of unknown cause until 14-years-old, but no history of immunodeficiency. T1-weighted magnetic resonance (MR) imaging showed a hypointense lesion with a hyperintense part, and ring-like enhancement with gadolinium-diethylenetriaminepenta-acetic acid (Gd-DTPA), in the left temporal lobe. T2-weighted and diffusion-weighted MR imaging showed the lesion surrounded by moderate hyperintense areas. He underwent gross total resection of the lesion. Histological examination demonstrated intracellular clusters of small basophilic spore-like bodies in the astrocytes, suggestive of microsporidia-infected astrocytes. However, immunohistochemical, polymerase chain reaction, and serological analyses failed to confirm the definitive diagnosis of microsporidiosis, so that he received no further treatment. Three years later, he presented with sensory disturbance in the left side of his face and left cerebellar ataxia, followed by fever, abnormal sensation in the left side of his face, and aggravated ataxia of the left upper and lower extremities on day 10 after admission. T1-weighted MR imaging with Gd-DTPA showed an enhanced lesion with irregular margin in the left cerebellar peduncle. T2-weighted MR imaging showed a diffuse hyperintense region around the lesion. Cerebrospinal fluid culture, serological analysis for autoimmune disease, and thoracic, abdominal, and pelvic computed tomography and 18F-fluorodeoxyglucose-positron emission tomography detected no abnormalities such as cancers or other lesions in the extracranial organs. No definitive diagnosis was obtained, but recurrence of microsporidiosis was the most probable cause. Administration of albendazole (600 mg/day) was started on day 15, because of rapid neurological and radiological deterioration. This treatment resulted in clinical improvement and disappearance of the lesion on MR imaging after daily administration for 4 weeks. He was discharged on foot with moderate sensory disturbance in the left side of the face and ataxia. Based on the clinical course and negative findings, the final diagnosis was microsporidiosis. This case suggests that microsporidiosis in the central nervous system can persist even in immunocompetent patients without involvement of any other organs, and that albendazole administration is likely to be effective.
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PMID:[Multiple intracerebral enhanced lesions strongly suspected to be microsporidiosis. A case report]. 1863 8

Relapsing polychondritis (RP) is a rare, generalized autoimmune disorder that is characterized by recurrent inflammation of various cartilaginous structures. Involvement of the central nervous system is rarely observed in RP. Here we report a case of encephalitis associated with RP. A 60-year-old man presented with headache and bilateral ear swelling. Three weeks later, he came to our hospital because of the acute onset of a speech impediment. A non-contrast computed tomography scan of the head showed slight high-density areas in his left frontal lobe, but he refused to be admitted and went home. On the next day, he developed acalculia, agraphia, right-left disorientation, and mild right hemiparesis. Brain MRI revealed hyperintensity areas in the left frontal sulcus on fluid-attenuated inversion recovery (FLAIR) images, and these hyperintensity areas were enhanced by gadolinium. Therefore, the patient's symptoms were diagnosed as focal epilepsy caused by meningoencephalitis. Other examinations, including laboratory blood tests, cerebrospinal fluid tests, and a cerebral angiography, were all negative. Therefore, a brain biopsy of the left frontal cortex was performed 5 days after the patient's admission. Pathological findings revealed chronic inflammation of the meninges, so prednisone was administered. After receiving oral prednisone, the patient's bilateral ear swelling dramatically improved and the lesions apparent on cranial MRI gradually subsided. The patient was diagnosed with RP by a neurologist after discharge from the hospital. In this study, early diagnosis and steroid treatment is recommended for patients with neurological complications due to RP.
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PMID:[Relapsing polychondritis presenting as encephalitis]. 2239 54

A 68-year-old man was referred to our hospital with tension-type headaches and a 1-year history of dementia. On neurologic examination, he had ideomotor apraxia and incomplete Gerstmann syndrome that was characterized by acalculia, agraphia, and finger agnosia. On imaging, multiple cystic lesions reported as "unusually dilated perivascular spaces" were observed along the medullary arteries in the left hemisphere; some of them had adjacent hyperintense areas in fluid attenuated inversion recovery images. We assumed that the multiple cystic lesions caused his higher cerebral dysfunction, because ideomotor apraxia and Gerstmann syndrome are usually indicative of a left parietal lobe lesion. MR spectroscopy in the lesion site revealed increased lactate. On MR angiography, the left middle cerebral artery and the left posterior cerebral artery were poorly visualized without localized stenosis. Technetium-99 bicisate single-photon emission computed tomography showed severely decreased cerebral blood flow in the left hemisphere. Electroencephalography showed slow waves in the left hemisphere.
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PMID:[A 68 year-old man presenting ideomotor apraxia and incomplete Gerstmann syndrome with multiple cystic lesions in the left hemisphere]. 2298 5

At present new daily persistent headache is just a group of conditions that are connected based on the temporal profile of their mode of onset. If new daily persistent headache is a true distinct syndrome like migraine then we need to start to define subtypes that have specific effective treatments such has been noted for migraine sub-forms. We present what we believe is the first recognized subtype of new daily persistent headache that which starts with a thunderclap headache onset. A patient presented with a 13 month history of a daily headache from onset which initiated as a thunderclap headache along with persistent acalculia. All neuroimaging studies for secondary causes were negative. Nimodipine rapidly and completely alleviated her headache and associated neurologic symptoms. We propose that this subtype of new daily persistent headache is caused by a very rapid increase in CSF tumor necrosis factor alpha levels leading to cerebral artery vasospasm with a subsequent thunderclap headache, then continuous or near continuous cerebral artery vasospasm leading to a persistent daily headache. Nimodipine which not only inhibits cerebral artery vasospasm but also tumor necrosis factor alpha production appears to be a specific treatment for this distinct subtype of new daily persistent headache.
J Headache Pain 2013 Dec 23
PMID:New daily persistent headache with a thunderclap headache onset and complete response to nimodipine (a new distinct subtype of NDPH). 2436 90