Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0011168 (dysphagia)
 15,644 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A 55-year-old woman noticed progressive hearing loss, earache and tinnitus in the left side in December 1988, followed by dysesthesia of the left face and hypogeusia. Those symptoms did not respond to the otological treatment of otitis media. In addition, the left eyelid ptosis, double vision and dysphagia appeared in May 1989. On admission, cranial nerves from III to XII were affected exclusively in the left side. The cell counts and the protein levels in the CSF were elevated. The MRI of the head showed hypertrophic dura mater at the left base of the skull covering the temporal lobe. No bone destruction was found in CT. The biopsy revealed the thickened dura mater with microabscess containing Langhans giant cells and lymphocytes. A diagnosis of pachymeningitis was made. After the therapy with antibiotics and then with prednisolone for several months, cranial nerve disturbances disappeared except hearing loss with decrease in cell counts and protein levels of the CSF. The follow-up MRI after one year showed decrease in thickness of dura mater. The MRI, particularly using enhancement with Gd-DTPA, was useful to make a diagnosis of hypertrophic pachymeningitis. It is suggested that the administration of antibiotics should be considered in the treatment of the pachymeningitis even if the causative agents were not identified.
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PMID:[A case of Garcin's syndrome caused by pachymeningitis secondary to otitis media, responsive to antibiotic therapy]. 176 59

We report a patient with syringobulbia extending to the pons, who could not open his mouth widely. He had been involved in the traffic accident at 16 years of age. Since them he had suffered numbness in the left neck and arm. At age 30, he became unable to open the mouth widely with pain in the left jaw joint. He also noted dysphagia and tinnitus. Neurologically, there were vocal cord paresis, dysesthesia of the face, ageusia and cerebellar ataxia all on the left side. Brain MRI revealed syringobulbia which extended to the pons. Spinal MRI revealed syringomyelia through the entire spinal cord. The syrinx of the spinal cord seemed to connect with the brainstem lesion. EMG of the masticatory muscles revealed paradoxical activity in the left masticatory muscles. We concluded that disturbance of jaw-opening in this case was caused by syringobulbia, the lesion of which could involve masticatory central pattern generator in the brainstem.
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PMID:[Disturbance of jaw-opening due to extension of syringobulbia to the pons--a case report]. 1260 83

Twenty-seven patients with ossification of the anterior longitudinal ligament (OALL) in diffuse idiopathic skeletal hyperostosis (DISH) in the cervical region were diagnosed among 2000 individuals during 10 months and analyzed clinically and radiologically by two neurosurgeons. Sex distribution was 20 men and 7 women with ages ranging from 57 to 82 years (average: 72.3 y.o.). Main signs and symptoms were dysesthesia of the upper extremities, stiff neck, dizziness and dysphagia (33%). Three patients had diabetes mellitus, 14 had hypertension, and 15 had hyperuremia. Ossification of the posterior longitudinal ligament (OPLL) co-existed in 18 patients (66%). Number of vertebral bodies with cervical OALL ranged from 4 to 6 (average: 4.8) and thickness of ossification of the anterior longitudinal ligament was from 2 to 6 (average: 3.1) mm. Originally we divided OALL in the cervical region into 3 types, nodular-type; 16 cases, continuous-type; 7 cases, and mixed-type; 4 cases. Small OPLL can be diagnosed by either cervical CT or myelo-CT. DISH is thought to be a benign clinical entity, but patients with OALL in DISH, accompanied by OPLL and those accompanied by dysphasia are frequently encountered and sometimes may be treated surgically.
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PMID:[Clinical and radiological study of ossification of the anterior longitudinal ligament in the cervical spine]. 1270 22

We report a 56-year-old Japanese man who was admitted because of dysphagia and left side facial dysesthesia. On admission, his general conditions were unremarkable. Neurological examination revealed that he was alert and well oriented. He exhibited left-side cranial nerve involvement such as the trigeminal(sensory and motor), glossopharyngeal and potential vagal nerve palsy. He exhibited neither long-tract signs, such as motor weakness, sensory disturbance in his exremities and pathological reflex, nor ataxia. By a few days after admission, his symptoms had worsened. Vertigo and diplopia appeared, and his consciousness level became drowsy. Bilateral third and sixth nerves, left fourth, fifth, eighth, ninth and tenth nerves were involved. Results of laboratory tests and CSF studies were within normal. Results of examination of the skull base X-ray and MRIs of the brain were normal. Administration of corticosteroid and intravenous administration of a high dose of gamma-globulin were not effective. His symptoms gradually recovered three months after admission. Based on clinical symptoms and results of physiological examination, i.e., an involvement of his consciousness and abnormal findings in blink reflex test that suggest involvement of the brainstem, he was diagnosed as having brainstem encephalitis. Although the exact pathophysiological mechanisms were unclear, it is clinically important to note that an atypical brainstem encephalitis may present a subacute progressive appearance of unilateral multiple cranial nerve palsies mimicking Garcin syndrome.
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PMID:[Unilateral multiple cranial nerve palsies mimicking Garcin syndrome as an atypical symptom of brainstem encephalitis: a case report]. 1275 38

A 75-year-old man was admitted to our hospital with dysesthesia of the right lip, dysphagia and gait disturbance. He presented with right Wallenberg syndrome and brain MR image showed a fresh infarction in the right lateral medulla. Therapy with heparin and ozagrel sodium was started. For a time his symptom improved a little, but after 8 days he developed re-infarction, thrombocytopenia and DIC, while being treated with heparin for cerebral infarction. Heparin was discontinued, and these symptoms improved quickly. The clinical course and the positive anti-platelet factor 4-heparin complex antibody suggested that these symptoms were caused by heparin-induced thrombocytopenia (HIT). HIT should be included as a differential diagnosis for progression of ischemic stroke under heparin therapy.
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PMID:[A case of heparin-induced thrombocytopenia that worsened preexisting cerebral infarction]. 1551 11

We describe an autopsy case of MM1-type sporadic Creutzfeldt-Jakob disease (CJD), the duration of which was 93 days. The patient was a 59-year-old Japanese man with no family history of prion disease or known iatrogenic exposure to CJD. His first symptom was dysesthesia in the left arm, suggestive of cervical cord involvement, and he showed rapidly progressive neurologic signs, such as dysarthria, dysphagia, lethargy, sleep apnea and respiratory failure, suggestive of brainstem involvement. Progressive mental deterioration combined with episodes of myoclonic seizure and periodic synchronous discharges on the electroencephalogram were observed in the later disease stage. Autopsy showed typical spongiform change to be wide-spread in the cerebral and cerebellar cortices, thalamus and basal ganglia. Synaptic-type PrP deposition was marked in the cerebral cortex, thalamus and basal ganglia. In the cerebellum, although the granular, molecular and Purkinje cell layers were well preserved from neuronal loss and gliosis, PrP deposition was marked in the molecular and granular cell layers. Spongiform degeneration and neuronal loss were not seen in the brainstem and spinal cord, but relatively marked PrP deposition was observed in the quadrigeminal body, substantia nigra, pontine nucleus, inferior olivary nucleus and posterior horn. Immunohistochemical staining for HLA-DR showed proliferation of activated microglia in the cerebral and cerebellar cortices, pontine nucleus, inferior olivary nucleus and posterior horn. The mechanisms underlying the neurologic symptoms and signs were unclear, but we speculate that, in addition to widespread involvement of the cerebral cortex, PrP deposition and microglial activation in the brainstem and spinal cord were responsible.
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PMID:Autopsy case of sporadic Creutzfeldt-Jakob disease presenting with signs suggestive of brainstem and spinal cord involvement. 1720 92

We report the first non-Caucasian case of facial onset sensory and motor neuronopathy (FOSMN) syndrome partially responding to various immunotherapies. A 55-year-old man had first felt paresthesia on his right cheek at age 45. This gradually extended to the scalp. Paresthesia of bilateral fingers and dysphagia appeared 6 years later. On admission, facial sensory impairment and bulbar palsy were found. There were no sensory or motor deficits evident in any limb, except for decreased deep tendon reflex and vibratory sensation. Videofluorography (VF) revealed decreased pharyngeal clearance. The sensory nerve action potential (SNAP) amplitudes of median and ulnar nerves were decreased. Intravenous immunoglobulin therapy and plasma exchange ameliorated his dysesthesia and dysphagia after several weeks, and resulted in improvements in VF and SNAP abnormalities. These observations suggest that FOSMN syndrome maybe, in part, immune-mediated.
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PMID:Facial onset sensory and motor neuronopathy (FOSMN) syndrome responding to immunotherapies. 1872 28

We report a case of a 46-year old man with acute autonomic, sensory and motor neuropathy (AASMN). He developed severe orthostatic hypotension, anuria,anhydrosis, tonic pupil with dysarthria, dysphagia, jaw claudication, and dysesthesia and sharp pain several days after symptom of upper respiratory infection. Neurological examination revealed severely decreased superficial sensation with normal deep sensation. Brain MRI findings showed bilateral trigeminal nerve swelling with gadolinium (Gd) enhancement. His motor and sensory symptoms and MRI abnormality were improved after the administration of intravenous immunoglobulin and intravenous methylprednisolone therapy; however his autonomic symptoms scarcely reacted to these immunotherapies. As long as we investigated in AASMN cases, bilateral trigeminal nerve swelling with Gd enhancement and dissociation between superficial and deep sensation disturbance have not reported, suggesting that the present case mainly disrupted C nerve fibers distributing postganglionic autonomic and temperature-pain sensory nerves.
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PMID:[A case of acute autonomic, sensory and motor neuropathy with swelling and gadolinium enhancement of bilateral trigeminal nerve on MRI and dissociation between superficial and deep sensation disturbance]. 2347 Aug 93

Tonsillar metastatic small cell lung cancer (SCLC) is rare, while anti-Hu antibodies are frequently found in SCLC. A 66-year-old man was admitted to our hospital with painful dysesthesia and muscle weakness in the distal extremities for over 1 year, progressive dysphagia for over 1 month, and severe cough and dyspnea for over 1 week. He was diagnosed with SCLC accompanied by tonsillar metastasis and anti-Hu antibody-associated paraneoplastic sensory neuropathy (PSN). The patient tolerated 6 cycles of sequential chemoradiotherapy and gradually recovered. The patient's disease remained in remission 2 years after the diagnosis with a remarkable reduction of tumor burden and a persisting high titer of anti-Hu antibodies. To our knowledge, this is the first case of tonsillar metastatic SCLC accompanied by anti-Hu antibody-associated PSN, whereby the anticancer immune response was presumed to play a vital role in disease control. Unilateral tonsillar metastasis of SCLC accompanied by anti-Hu antibody-associated PSN can occur and in certain circumstances, may have a favorable prognosis.
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PMID:Small Cell Lung Cancer Accompanied by Tonsillar Metastasis and Anti-Hu Antibody-Associated Paraneoplastic Neuropathy: A Rare Case Report With Long-Term Survival. 2668 64

A 65-year-old man with a history of Wallenberg syndrome caused by vertebral artery dissection at 62 years old was admitted to our hospital with nausea, vertigo, right facial dysesthesia, right hemiplegia, crossed sensory disturbance (sensory loss and numbness in the right face and left body below the neck), and right limb ataxia. Magnetic resonance imaging (MRI) performed 80 minutes after onset revealed no acute ischemic stroke lesions, but magnetic resonance angiography (MRA) demonstrated complete occlusion of the right vertebral artery. Based on these neurological and MRA findings, atypical lateral medullary infarction was suggested, and intravenous tissue plasminogen activator (IV-tPA) was started 178 minutes after onset. Right hemiplegia improved immediately after IV-tPA administration. MRI performed on hospital day 2 showed an acute ischemic lesion on the right side of the medulla oblongata, resulting in a diagnosis of Opalski syndrome. Opalski syndrome is a rare subtype of Wallenberg syndrome accompanied by hemiplegia of the side ipsilateral to the lesion, and expansion of the stroke lesion to the corticospinal tract below the pyramidal decussation is considered to cause ipsilateral hemiplegia. Based on this case and previous reports, Opalski syndrome should be considered when limb ataxia and crossed sensory deficit are observed among patients with hyperacute-onset hemiplegia, and IV t-PA therapy should be considered even in the absence of neurological findings such as dysphagia, dysarthria, and Horner's signs and radiological evidence of acute ischemic stroke.
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PMID:Opalski Syndrome Treated with Intravenous Recombinant Tissue Type Plasminogen Activator-Case Report and Review of Literature. 3243 29


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