Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0011570 (depression)
 172,036 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

1. Normal pressure hydrocephalus (NPH) is a rare but potentially treatable form of dementia. Shunting will improve functioning in 40% to 50% of patients. 2. The classic symptoms of NPH are dementia characterized by mild memory impairment and apathy, ataxic gait, and urinary hesitancy or incontinence. 3. The patient with NPH may present with psychiatric symptoms of depression, paranoia, visual hallucinations, irrational hostility, and aggression or mania. 4. Patients with NPH are indifferent about activities of daily living and personal safety and require close supervision.
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PMID:Normal pressure hydrocephalus. A potentially reversible form of dementia. 161 84

A 68-year-old man was admitted to our hospital because of numbness in the hands and feet, and unsteady gait in August, 1986. On neurological examination, deep tendon reflexes were absent in all limbs without pathological reflexes. Superficial and deep sensory disturbances of a glove and stocking type up to the level of the elbow and the knee were observed. Pseudoathetosis was noted in the hands. His gait was ataxic and Romberg sign was positive. Muscle strength was slightly decreased. Sural nerve biopsy showed severe loss of large myelinated fibers. Laboratory studies for malignancy showed lung cancer (Squamous cell carcinoma). Left pneumonectomy was performed in November, 1986, but he died in March, 1987. At autopsy, neither metastasis nor direct infiltration of malignant cells in the central and peripheral nervous systems were present macroscopically and histopathologically. Degeneration of the dorsal root ganglion and the posterior columns of the spinal cord were remarkable. Since 1955, only 9 cases of subacute sensory neuropathy had been reported in Japan. We analysed 10 Japanese cases (including our case) to clarify the clinicopathological features of subacute sensory neuropathy. Clinically, ataxic gait, paresthesia, deep sensory disturbance, and depression of deep tendon reflexes were present in the majority of the cases. Neuropathologically, neuronal cell loss and degeneration of the dorsal root ganglion, posterior roots and posterior columns of the spinal cord were universal findings.
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PMID:[Subacute sensory neuropathy associated with carcinoma--an autopsy case report and an analysis of Japanese cases]. 217 56

The authors report the clinical review of 20 childhood cases with Friedreich's ataxia. The mean age at onset of symptoms was 6.1 years. The main presenting symptom was abnormal gait (100%). Ataxia of gait and limbs and depressed or absent tendon reflexes were found in all cases. Clinical findings are in accordance with the findings of Harding and Werdelin. Neurophysiological studies (especially sensory) are important in the confirmation of the diagnosis. Of the 10 cases in which sensory nerve conduction velocity measurements were performed, 7 had absent sensory action potentials, 2 had decreased potentials and one was normal. In our study, it is shown that in patients having ataxic gait, ataxia of limbs and tendon reflexes depression or loss, Friedreich's ataxia may be diagnosed with the help of electrophysiological studies.
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PMID:Friedreich's ataxia: a clinical review of 20 childhood cases. 340 87

The effects of sodium iodate (SI), iodoacetic acid (IAA) and ethambutol (EB) on the electroretinogram (ERG) and the visual evoked potential (VEP) were examined in unrestrained rats. A single intravenous dose of SI at 25 mg/kg caused depression of amplitudes of the ERG a-wave and oscillatory potentials 24 hrs after dosing. Following these changes, the amplitude of the ERG b-wave decreased. The depression of the VEP was observed in parallel with the depression in amplitude of the ERG. A single intravenous dose of IAA, even at a dose of 60 mg/kg which induced death of the rats, did not cause any significant abnormality in the ERG and VEP. Repeated subcutaneous dose of EB at 500 mg/kg/day depressed the amplitude of the P1-N1 wave and prolonged the peak latency of the P1 and N1 waves of the VEP without affecting the ERG after administration for 5 to 6 weeks. These abnormalities of the VEP appeared almost in parallel with ataxic gait. Neither gross behavioral changes suggesting visual disturbances nor abnormal ocular fundus was revealed in any rat receiving SI or EB even when marked depression of the ERG and/or VEP was observed. These results indicate that SI damages retinal function and EB does the conduction pathways from the retina to the visual cortex. In addition, the simultaneous recordings of both the ERG and VEP in unrestrained rats were found to be useful for evaluating the visual toxicity, and to furnish useful information on the site of toxic action of drugs.
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PMID:[Effects of sodium iodate, iodoacetic acid and ethambutol on electroretinogram and visual evoked potential in rats]. 652 94

Previous studies, which have demonstrated that carbamazepine (CBZ) possesses direct muscle spindle suppressant activity, suggest that CBZ may have therapeutic value in the treatment of hypertonic disorders characterized by high fusimotor drive. The effects of CBZ on motor tone in the midcollicular decerebrate cat were therefore examined. CBZ, in a concentration-dependent manner, reduced muscle tone, as measured by the force necessary to overcome hyperextension. Significant depression was first observed at a serum concentration of about 25 micrograms/ml, whereas 50% depression occurred at about 40 micrograms/ml. These effects could not be attributed to the hypotensive effect of the drug. CBZ produced little or no effect on spontaneous gamma motoneuron activity recorded in teased ventral roots of segmentally deafferented spinal cords of decerebrate animals; chlorpromazine, however, was effective in suppressing such activity. In the same preparations, CBZ reduced polysynaptic but had little effect on monosynaptic spinal reflexes evoked by dorsal root stimulation. The drug also shortened the duration of the pause in spontaneous gamma motoneuron activity after dorsal root stimulation. Serum concentrations which diminished extensor rigidity in decerebrate cats induced mild to moderate intoxication in intact unanesthetized cats. This was characterized by ataxic gait, sedation and hypotonia. These experiments indicate that CBZ may be of value alone or adjunctively in the reduction of some forms of muscle hypertonicity.
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PMID:Effects of carbamazepine on muscle tone in the decerebrate cat. 682 68

The acute toxicity of diethyl 4-(benzothiazol-2-yl)benzylphosphonate (KB-944) was studied in mice, rats and dogs: In mice and rats, toxic symptoms such as deceleration of spontaneous movement, ataxic gait, disappearance of righting reflex, reduction in body temperature and suppression of breathing appeared following administration of a single dose of KB-944. The symptoms developed in dogs were depression, bradycardia and labored breathing. The LD50 values determined in male and female rats were 1622 and 1555 mg/kg, respectively, for oral administration, 2216 and 2820 mg/kg for subcutaneous injection, and 762 and 479 mg/kg for intraperitoneal injection. The LD50 values determined in male and female mice were 2807 and 3856 mg/kg, respectively, for oral administration, greater than 4000 mg/kg for subcutaneous injection, and 815 and 777 mg/kg for intraperitoneal injection. As shown above, there was no evident difference in LD50 between sexes in either species of animals. Since many of the dogs given an oral dose larger than 1000 mg/kg vomited the drug, oral LD50 value could not be determined.
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PMID:Acute toxicity study of KB-944, a new calcium antagonist. 689 Aug 28

mGluR1 mutant mice are viable but show characteristic cerebellar symptoms such as ataxic gait and intention tremor. The anatomy of the cerebellum is not overtly disturbed. Excitatory synaptic transmission from parallel fibers (PFs) to Purkinje cells and that from climbing fibers (CFs) to Purkinje cells appear to be functional, and voltage-gated Ca2+ channels of Purkinje cells are normal. Both PF and CF synapses display normal short-term synaptic plasticity to paired stimuli. By marked contrast, long-term depression (LTD) is clearly deficient and conditioned eyeblink response is impaired. We conclude that mGluR1 is required for the induction of LTD and that the ataxic behavior and impaired eyeblink conditioning of the mGluR1 mutant mice are primarily due to deficient LTD.
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PMID:Deficient cerebellar long-term depression and impaired motor learning in mGluR1 mutant mice. 795 3

A 50 year-old woman presented in January of 1995 with a prolonged history of symptoms of multiple sclerosis (MS) and was classified at the time with a remitting-progressive course. Her chief symptoms included slurring of speech, impairment of vision with intermittent diplopia, difficulties with gait and balance with spastic-ataxic gait, mental depression, insomnia, fatigue, impaired cognitive functions notably poor short term memory and recurrent urinary tract and sinus infections. An MRI scan showed multiple nodular demyelinating lesions scattered in the subcortical white matter and periventricularly of both cerebral hemispheres. Over the following 18 months, while receiving three treatment sessions per week with picotesla electro-magnetic fields (EMFs) which were applied extracranially, she showed a significant recovery in both physical and mental symptoms and additionally experienced decreased susceptibility to infections. In addition, the course of her disease appeared to have stabilized as opposed to the preceding 5 years during which time she experienced insidious, steady deterioration in her functioning. Despite this remarkable clinical recovery through the application of EMFs, and MRI scan obtained at the same diagnostic center 18 months after initiation of treatment with EMFs showed no changes in the number and size of the demyelinating plaques. These findings demonstrate lack of a correlation between recovery of symptoms and the number and extent of demyelinating plaques on MRI scan. It has been known since the days of Charcot in the latter half of the 19th century that in MS there is a great disparity between the histopathological changes of the disease and neurologic deficits. This report enhances the notion that demyelination may reflect an epiphenomenon of the disease.
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PMID:Lack of a correlation between demyelinating plaques on MRI scan and clinical recovery in multiple sclerosis by treatment with electromagnetic fields. 913 46

We report on a Japanese family having an autosomal dominant neurodegenerative disease with chromosomal instability and radiosensitivity. Clinical manifestations of affected members included short stature, osteoporosis, severe dental caries, and various neurological abnormalities, such as mental retardation, depression, dysarthria, hyperreflexia, and ataxic gait. MRI demonstrated a markedly atrophic spinal cord and degeneration of the white matter. Cytogenetic examination showed spontaneous chromosome rearrangements at 14q11.2 and hypersensitivity to radiation and bleomycin. The degree of these cytogenetic abnormalities was significantly higher in the patients than in normal controls but lower than in patients with ataxia telangiectasia or Nijmegen breakage syndrome. Moreover, genetic anticipation was observed in this family: the age of disease onset became earlier, MRI abnormalities more extensive, and the chromosome hypersensitivity to radiation increased in successive generations. We speculate that a basic defect in this family is a mutation in the gene that is responsible for DNA double-strand breakage repair.
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PMID:Japanese family with an autosomal dominant chromosome instability syndrome: a new neurodegenerative disease? 1103 37

There is nothing more discouraging than for a patient to be given a specific diagnosis, then to be told that there is nothing that can be done. Physicians are equally disheartened to see exponential progress being made in the understanding of the pathophysiology of a complex disorder but few direct benefits resulting for their patients. Over the past 5 years, molecular genetic research has completely revolutionized the way in which the progressive cerebellar ataxias are classified and diagnosed, but it has yet to produce effective gene-based, neuroprotective, or neurorestorative therapies. The treatment of cerebellar ataxia remains primarily a neurorehabilitation challenge, employing physical, occupational, speech, and swallowing therapy; adaptive equipment; driver safety training; and nutritional counseling. Modest additional gains are seen with the use of medications that can improve imbalance, incoordination, or dysarthria (amantadine, buspirone, acetazolamide); cerebellar tremor (clonazepam, propranolol); and cerebellar or central vestibular nystagmus (gabapentin, baclofen, clonazepam). Many of the progressive cerebellar syndromes have associated features involving other neurologic systems (eg, spasticity, dystonia or rigidity, resting or rubral tremor, chorea, motor unit weakness or fatigue, autonomic dysfunction, peripheral or posterior column sensory loss, neuropathic pain or cramping, double vision, vision and hearing loss, dementia, and bowel, bladder, and sexual dysfunction), which can impede the treatment of the ataxic symptoms or can worsen with the use of certain drugs. Treatment of the associated features themselves may in turn worsen the ataxia either directly (as side effects of medication) or indirectly (eg, relaxation of lower limb spasticity that was acting as a stabilizer for an ataxic gait). Secondary complications of progressive ataxia can include deconditioning or immobility, weight loss or gain, skin breakdown, recurrent pulmonary and urinary tract infections, aspiration, occult respiratory failure, and obstructive sleep apnea, all of which can be life threatening. Depression in the patient and family members is common. Although no cures exist for most of the causes of cerebellar ataxia and there are as yet no proven ways to protect neurons from premature cell death or to restore neuronal populations that have been lost, symptomatic treatment can greatly improve the quality of life of these patients and prevent complications that could hasten death. Supportive interventions should always be offered-- education about the disease itself, genetic counseling, individual and family counseling, referral to support groups and advocacy groups, and guidance to online resources. Misinformation, fear, depression, hopelessness, isolation, and financial and interpersonal stress can often cause more harm to the patient and caregiver than the ataxia itself.
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PMID:Cerebellar Ataxia. 1109 49


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