Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0004134 (ataxia)
 15,886 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The effect of TRH on cerebral blood flow in patients with spinocerebellar degeneration and cerebrovascular disease was investigated. Cerebral blood flow was measured by the 133Xenon arterial injection method before, and 30 min after, the intravenous administration of 1000 micrograms of TRH. TRH had no effect on mean arterial blood pressure in either group. In the spinocerebellar degeneration group, cerebral blood flow increased slightly after the injection of TRH, from 52.7 +/- 10.5 to 56.7 +/- 16.0 ml/100 g brain/min. In two patients with spinocerebellar degeneration, whose autonomic function was normal and whose brainstem structure appeared normal in the CT scan, cerebral blood flow increased from 54.8 to 66.4 ml (21.2%), and from 68.6 to 79.9 ml (16.5%), respectively. In the patients with cerebrovascular disease, cerebral blood flow did not change (49.7 +/- 10.8 ml before and 49.4 +/- 12.6 ml after TRH). Cerebral blood flow reportedly increases following an intravenous injection of TRH in animals, supposedly due to the activation of intrinsic cerebral vasodilative fibers situated in the submesencephalic brainstem region. Our results are consistent with this hypothesis and with the clinical finding that TRH especially improves ataxia in spinocerebellar degeneration where there is no pyramidal involvement or disorder of deep sensation.
 ...
PMID:Effect of thyrotropin-releasing hormone (TRH) on cerebral blood flow in spinocerebellar degeneration and cerebrovascular disease. 895 61

Patients with multiple sclerosis sometimes show subthalamic lesions presenting syndrome of inappropriate secretion of ADH (SIADH), hypothermia, hyperprolactinemia, weight loss, and cachexia. Hyperprolactinemia also has been found in the patients with active systemic lupus erythematosus, because prolactin can be produced from human activated lymphocytes. We described a case of multiple sclerosis showing galactorrhea-amenorrhea syndrome with hyperprolactinemia. A 31-year-old woman showed a high level of prolactin in the serum (79.6 ng/ml) during remission stage 5 months after the onset of multiple sclerosis. She showed galactorrhea-amenorrhea syndrome 3 years later. She showed dysesthesia in her limbs, relapsing monoparesis, visual disturbance and Gd-enhanced plaques in Brain MRI for 6 years. She was admitted to our hospital on November 24, 1995. A neurological examination showed hyporeflexia of the upper extremities, hyperreflexia of the lower extremities, bilateral ankle clonus, truncal ataxia, and neurogenic bladder. Laboratory tests revealed increased level of serum prolactin, exaggerated secretion of serum prolactin after intravenous injection of 500 micrograms TRH, and marked suppression after oral administration of 2.5 mg bromocriptine. Brain MRI showed demyelinating lesions near the lateral ventricle, and cervical MRI (T2 image) showed high signal intensity lesions in the spinal cord from C2 to C5. In the previous case, galactorrhea-amenorrhea syndrome was found during the exacerbation stage of multiple sclerosis. Hyperprolactinemia may be caused from subthalamic lesions or by activated lymphocytes in multiple sclerosis. We considered that hyperprolactinemia and galactorrhea-amenorrhea syndrome in our patient might be caused from subthalamic lesions because lymphocytes were not activated during the remission stage of multiple sclerosis.
 ...
PMID:[A case of multiple sclerosis with galactorrhea-amenorrhea syndrome]. 936 74

1 Nootropic drugs increase glucose uptake into anaesthetised brain and into Alzheimer's diseased brain. Thyrotropin-releasing hormone, TRH, which has a chemical structure similar to nootropics increases cerebellar uptake of glucose in murine rolling ataxia. This paper shows that nootropic drugs like piracetam (2-oxo 1 pyrrolidine acetamide) and levetiracetam and neuropeptides like TRH antagonise the inhibition of glucose transport by barbiturates, diazepam, melatonin and endogenous neuropeptide galanin in human erythrocytes in vitro. 2 The potencies of nootropic drugs in opposing scopolamine-induced memory loss correlate with their potencies in antagonising pentobarbital inhibition of erythrocyte glucose transport in vitro (P<0.01). Less potent nootropics, D-levetiracetam and D-pyroglutamate, have higher antagonist Ki's against pentobarbital inhibition of glucose transport than more potent L-stereoisomers (P<0.001). 3 Piracetam and TRH have no direct effects on net glucose transport, but competitively antagonise hypnotic drug inhibition of glucose transport. Other nootropics, like aniracetam and levetiracetam, while antagonising pentobarbital action, also inhibit glucose transport. Analeptics like bemigride and methamphetamine are more potent inhibitors of glucose transport than antagonists of hypnotic action on glucose transport. 4 There are similarities between amino-acid sequences in human glucose transport protein isoform 1 (GLUT1) and the benzodiazepine-binding domains of GABAA (gamma amino butyric acid) receptor subunits. Mapped on a 3D template of GLUT1, these homologies suggest that the site of diazepam and piracetam interaction is a pocket outside the central hydrophilic pore region. 5 Nootropic pyrrolidone antagonism of hypnotic drug inhibition of glucose transport in vitro may be an analogue of TRH antagonism of galanin-induced narcosis.
 ...
PMID:Piracetam and TRH analogues antagonise inhibition by barbiturates, diazepam, melatonin and galanin of human erythrocyte D-glucose transport. 1514 55


<< Previous 1 2