Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0013362 (dysarthria)
 3,768 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Patients with amyotrophic lateral sclerosis (ALS) have symptoms of progressive muscle weakness, of disturbed speech and swallowing, and in the terminal phase those of respiratory weakness. Treatment options, in particular those for excessive weight loss and respiratory weakness, should be introduced to the patients and their families when the patient is emotionally capable and before dysarthria severely hampers communication. Special equipment for keeping the patient as mobile as possible should be made available much earlier than in the case of other diseases of the muscles as in ALS progression is much faster. Cramps, pathological crying or laughter, spasms, and spasticity can all be treated by medication. When speech can no longer be understood, adaptive strategies such as sign language, mime, posture and communication apparatus varying from a note pad to advanced computer systems can be used. Sialorrhoea, caused by difficulty swallowing with its accompanying danger of aspiration can be halted by the use of medication, by radiotherapy and by the injection into the salivary glands of botulin A toxin. Weight loss, also a result of dysphagia, can be avoided by eating frequent small meals or if necessary performing a percutaneous endoscopic or radiological gastroscopy. Excess mucus in the respiratory tract can be treated with anticholinergics. Difficulty in coughing up thick and sticky mucus cannot always be adequately helped. Respiratory weakness is treatable by external respiratory supportive therapy using a nasal mask, as well as invasive respiratory support via a trachcostoma and by treating the symptoms of respiratory weakness. The latter form of treatment is palliative and forms part of terminal care. During the terminal phase restlessness, anxiety, pain, and dyspnoea require the most attention. Treatment requires careful multidisciplinary cooperation.
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PMID:[The symptomatic treatment of amyotrophic lateral sclerosis]. 1519 69

We report a 69-year-old man with pure ataxic speech. He was admitted to the surgical ward of our hospital because of exercise-induced pain in the right arm. He underwent angiography of the right arm, and was discharged the next day. When he returned home, he exhibited an acute-onset dysarthria. He was admitted to our neurology ward the next day because the dysarthria did not improve. On admission, neurological examinations revealed moderately ataxic speech, but other neurological findings were within normal limits. Cranial MRI revealed an infarct localized from the lobulus simplex to the lobulus quadrangularis in the right cerebellum. Three cases of pure dysarthria due to cerebellar infarction have been reported previously. We compared cerebellar lesions in the 4 cases of pure dysarthria due to cerebellar infarction. Since the lobulus simplex of the upper cerebellar hemisphere was involved in all 4 cases, we speculated that ataxic speech occurred from the impairment of this cerebellar area.
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PMID:[A case of cerebellar infarction with pure dysarthria]. 1519 61

Miller-Fisher syndrome (MFS) typically presents with ophthalmoplegia, ataxia, and areflexia. Atypical MFS additionally includes bulbar impairment, affection of the limbs, or abortive presentations. Mostly, MFS follows an infection with Campylobacter jejunii. Aspergilloma has not been reported to trigger MFS. In a 48-year-old male tiredness, tinnitus, otalgia, parietal hyperaesthesia, coughing, plugged nose, hypoacusis, globus sensation, epipharyngeal pain, dysarthria, hypogeusia, arthralgia, lid cloni, facial hypaesthesia and tooth ache consecutively developed. There were occasional lid cloni, left-sided facial hypaesthesia, reduced gag reflex, divesting soft palate, and absent tendon reflexes. CSF investigations revealed normal cell-count but increased protein. Antibodies against GM1 and GQ1b were negative. Atypical MFS was diagnosed. Otolaryngological examinations revealed chronic sinusitis maxillaris from an aspergilloma. After immunoglobulins and resectioning of the aspergilloma, neurological abnormalities disappeared within 19d. MFS may manifest as unilateral lower cranial nerve lesions without affection of the upper cranial nerves or ataxia. Atypical MFS may be triggered by parasinusoidal aspergilloma.
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PMID:Anti-GQ1b-negative Miller-Fisher syndrome with lower cranial nerve involvement from parasinusoidal aspergilloma. 1608 Nov 59

Amyotrophic lateral sclerosis (known in the UK as motor neuron disease) is a devastating illness with uncertain pathogenesis. In this Seminar, we review its natural history, clinical features, diagnostic criteria, variant and mimic syndromes, genetic forms, and epidemiology. Several hypotheses about causes of the disorder are discussed, such as excitotoxicity and oxidant stress, and we review past and present putative disease-modifying treatments. Disease-management strategies, from telling the patient about their illness to end-of-life decisions and palliative care, are presented. We review options for control of the main symptoms of amyotrophic lateral sclerosis--including dysphagia, dysarthria, respiratory distress, pain, and psychological disorders--and care in the terminal phase. The need for good psychosocial and spiritual care of patients and families is emphasised. We conclude with an overview of some current major issues and future prospects, ranging from the search for disease markers to challenging developments such as stem-cell and gene therapy.
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PMID:Amyotrophic lateral sclerosis. 1757 95

A 36 year old woman ruptured her right Achilles tendon in a skiing accident. Previous medical history is unremarkable except for a history of migraine for many years. She is married with three children with no history of spontaneous miscarriage. She smokes 15 cigarettes a day and takes the oral contraceptive pill. She is admitted to a local hospital where surgery to repair the Achilles tendon is performed followed by fitting of a plaster cast. Due to pain from the plaster cast she is slow to mobilise. On day 7 postoperatively she develops increasing pain in the right leg. When the plaster is removed the right calf is found to be painful, warm, and swollen. The next day while straining on the toilet she collapsed with left arm weakness. Clinical examination revealed dysarthria with pyramidal weakness of the left arm. The significance of these symptoms, the diagnosis, and the short and long term treatment of these postoperative problems are discussed in an interactive case presentation.
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PMID:Learning on the Web. Case 2: patent foramen ovale (PFO) and paradoxical embolism. 1806 45

A 34-year-old woman with a previous history of severe headache ("thunderclap") was admitted with a diagnosis of aneurysmal subarachnoid hemorrhage (SAH). The patient developed symptomatic vasospasm on day 5 that resolved rapidly after having increased arterial blood pressure. She experienced also short-lasting excruciating headache. On day 12, while velocities had normalised, as revealed by transcranial Doppler (TCD), for more than 48 h, she developed aphasia and right hemiplegia associated with diffuse segmental vasospasm on the left middle cerebral artery. Intra-arterial infusion of vasodilatory agents was required. Recurrence of symptomatic vasospasm was noted on day 25, with a great number of territories involved as shown in the cerebral angiogram. A second intra-arterial treatment was needed. The patient complained of multiple episodes of extremely severe headache ("thunderclap"), with also transient dysarthria and hemiparesia on day 30. She was discharged on day 38 after full recovery. The clinical and TCD/radiological findings were consistent with a reversible cerebral vasoconstriction syndrome overlapping SAH related symptomatic vasospasm.
J Headache Pain 2009 Aug
PMID:Possible overlap between reversible cerebral vasoconstriction syndrome and symptomatic vasospasm after aneurysmal subarachnoid hemorrhage. 1938 33

A 61-year-old man was admitted to our department with radicular back-pain and progressive gait-difficulties. On examination he had flaccid paraparesis and bladder-retention. He subsequently developed palsy of n. oculomotorius, dysarthria, right-sided Bells palsy and weakness of his right arm over a 4-week period. He became disoriented and died without a diagnosis. MRI of the brain and columna were negative. Extensive search for malignancies yielded negative results. Cytology specimens were inconclusive and repeated liquor-examinations showed very low glucose levels, mild pleocytosis, elevated protein. Autopsy revealed a small adenocarcinoma of the lung and meningeal carcinomatosis originating from the adenocarcinoma.
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PMID:[A 61-year-old man with sciatica]. 1944 55

A 39-year-old man who presented with unilateral proptosis and periocular pain rapidly developed reduced consciousness, facial numbness, dysarthria, and gait ataxia from a direct carotid-cavernous fistula (CCF) with drainage into posterior fossa veins. Brain MRI revealed abnormal signal throughout the brainstem, indicative of venous hypertension and edema. Closure of the fistula by detachable balloon eliminated the clinical and imaging abnormalities. This is the fifth reported case of brainstem complications of a direct CCF. It highlights potentially serious complications of this condition and their reversibility with prompt treatment.
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PMID:Direct carotid-cavernous fistula causing brainstem venous congestion. 1945 71

Sarcoidosis is a chronic disease of unknown aetiology. Neurosarcoidosis is registered in 5% of patients with sarcoidosis. Clinical manifestations of sarcoidosis are numerous and diverse. Manifestation of Neurosarcoidosis includes partial- and grand-mal seizures, low-grade fever, headache, increased intracranial pressure, visual disturbances, diabetes insipidus, amenorrhea- galacterorrhea syndrome and pituitary failure, hypogonadotropic hypogonadism, hyperprolactinemia, unilateral and bilateral facial palsy, infiltration of meninges (aseptic meningitis) and nerve roots, leptominingitis, pachymeningitis with cranial neuropathies, pseudotumor, mild cognitive disorder, psychosis, delirium, dementia, disorientation, amnesia, progressive visual deterioration and proptosis, axonal polyneuropathies, mononeuropathies, chronic polyradiculoneuritis, peripheral neuropathy, cranial nerve abnormalities, radiculopathies, peripheral neuropathy, mononeuritis multiplex, progressive numbness and deep sensation disturbance in bilateral lower extremities, hemiplegia, hyperreflexia with pathological reflexes and hypesthesia, upward gaze palsy, spinal cord compression, dysarthria, dysphagia, weakness, episodes of blurred vision, diplopia, intracerebral hemorrhage, neuro-ophthalmic manifestations, intranuclear ophthalmoplegia, dysorientation, vasculitis presenting with strokes, intracranial hypothalamic lesion, paresthesis, hemiparesis, myelopathy in the cervico-thoracic region, lumbar pain, sensory level and inability of lateral gaze (Tab. 2, Ref. 60).
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PMID:Clinical manifestations of neurosarcoidosis. 1982 43

Headache associated with moyamoya disease (HAMD) is common in moyamoya disease. However, the characteristics and classification of HAMD are largely unknown. We present a case of a 39-year-old woman with HAMD. To characterize and classify the features of this syndrome, the patient was asked to complete a 4-month diagnostic headache diary. There was a total of 15 ictal days. All episodes were without aura. The headache was more commonly pressing (10/15), mild to moderate in severity (14/15), unchanged by physical activity (11/15), and associated with photophobia (10/15). The International Headache Society Classification was utilized to determine that eight episodes met criteria for probable migraine without aura, while seven episodes met criteria for probable frequent episodic tension-type headache. We identified four other case reports of HAMD with partial descriptions of the characteristics. When combined with our patient, the median age was 34 years old (range 6-49, SD 16). Four were female, while the patient with cluster headache was male. The median time from headache onset to diagnosis with moyamoya disease was 9.5 months (range 0-192, SD 88.0). Headaches were described as migraine with aura in two of five cases, hemiplegic migraine in one of five, and cluster headache in one of five. The highest intensity was described as severe in three of three cases, in which headache intensity was reported. Meanwhile, nausea, vomiting, and photophobia were present in two of three cases, where these features were reported, while nausea without vomiting was seen in one of three cases. In all five cases, patients had other neurological symptoms, such as paresis, seizures, visual disturbances, dysarthria, allodynia, ptosis, and unilateral restless leg syndrome. In conclusion, HAMD can present as migraine without aura. It can be the first presenting symptom of moyamoya disease. The headache features are not diagnostic; hence, early neurovascular imaging should be considered in patients with new onset, refractory migraine-like headache, especially in the setting of other neurological symptoms to exclude underlying moyamoya disease. Further reports using headache diaries are needed to better characterize HAMD as well as to determine whether headache with tension-type features is also part of this condition.
J Headache Pain 2010 Feb
PMID:Headache associated with moyamoya disease: a case story and literature review. 2001 51


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