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Biomedical subjects

A Samii

Publications and source records attributed to A Samii.

46 records · Page 3Linked to original sources
PubMed1996

Abnormal cortical motor excitability in dystonia.

To assess the excitability of the motor system, we studied 11 patients with task-specific dystonia and 11 age-matched normal subjects. The dominant side was affected in nine of the patients. We delivered transcranial magnetic stimuli at different stimulus intensities and with different levels of muscle facilitation to the side contralateral to the side of electromyographic recording, and recorded motor evoked potentials (MEPs) from the flexor carpi radialis muscles bilaterally. The threshold intensity for eliciting MEPs at rest did not differ between patients and normal subjects. We compared the affected side in patients with the dominant side in normal subjects. With facilitation, the percentage of the area of the MEP to the M wave (MEP area%) was similar in both groups at low stimulus intensities, but with increasing stimulus intensity the increase in the MEP area% was greater in patients than in normal subjects (ANOVA, p < 0.001). The increase in MEP area% was similar in both groups with increasing facilitation levels. The duration of the silent period was similar in patients and normal subjects. We conclude that cortical motor excitability is increased in dystonia.

Adult↗
PubMed1996

Characterization of postexercise facilitation and depression of motor evoked potentials to transcranial magnetic stimulation.

We studied the effects of exercise on motor evoked potentials (MEPs) to transcranial magnetic stimulation (TMS) and transcranial electrical stimulation (TES). Subjects performed 30-second periods of isometric exercise of the extensor carpi radialis until fatigue, which was defined as the inability to maintain half maximum force. The amplitude of MEPs to TMS recorded from the resting muscle after each exercise period was on average more than twice the pre-exercise value (postexercise MEP facilitation). After fatigue occurred, the MEP amplitudes were approximately 60% of the pre-exercise value (postexercise MEP depression). There was a gradual recovery of the depressed MEPs to pre-exercise values over several minutes of rest. Postexercise MEP facilitation was constant when exercise intensity ranged from 10 to 50% of maximum voluntary contraction and it decayed to baseline over several minutes after the end of exercise. There was no postexercise MEP facilitation to TES. We hypothesize that both postexercise MEP facilitation and MEP depression are due to intracortical mechanisms.

Adult↗
PubMed1996

Decreased postexercise facilitation of motor evoked potentials in patients with chronic fatigue syndrome or depression.

We studied the effects of exercise on motor evoked potentials (MEPs) elicited by transcranial magnetic stimulation (TMS) in 18 normal (control) subjects, 12 patients with chronic fatigue syndrome, and 10 depressed patients. Subjects performed repeated sets of isometric exercise of the extensor carpi radialis muscle until they were unable to maintain half maximal force. MEPs were recorded before and after each exercise set and for up to 30 minutes after the last set. The mean amplitude of MEPs recorded from the resting muscle immediately after each exercise set was 218% of the mean pre-exercise MEP amplitude in normal subjects, 126% in chronic fatigue patients, and 155% in depressed patients, indicating postexercise MEP facilitation in all three groups. The increases in the patient groups, however, were significantly lower than normal. The mean amplitudes of MEPs recorded within the first few minutes after the last exercise sets in all three groups were approximately half their mean pre-exercise MEP amplitudes. This postexercise MEP depression was similar in all groups. We conclude that postexercise cortical excitability is significantly reduced in patients with chronic fatigue syndrome and in depressed patients compared with that of normal subjects.

Adult↗
PubMed1994

Administration of an omega-conopeptide one hour following traumatic brain injury reduces 45calcium accumulation.

The omega-conopeptide, SNX-111 (NEUREX Corporation) was administered to rats 1 hour following a lateral fluid percussion brain injury to determine if the drug could reduced the extent and duration of trauma-induced calcium accumulation. Administration at doses of 3 or 5 mg/kg (i.v.) markedly reduced the extent of calcium accumulation as determined using 45calcium autoradiography primarily within the cerebral cortex and hippocampus. The reduction of calcium accumulation was particularly event within the parietal cortex beginning as early as 6 hours and lasting out to 48 hours following injury. Although not as effective as in the cerebral cortex, SNX-111 did exhibit a reduction of calcium accumulation within the dorsal hippocampus especially at 24 and 48 hours after the insult. These preliminary results demonstrate that SNX-111 can reduce the injury-induced accumulation of calcium even when administered 1 hour after the insult and offers this compound as a potential therapeutic treatment for traumatic brain injury.

Animals↗
PubMed1994

Blood-brain barrier transport of neuropeptides: analysis with a metabolically stable dermorphin analogue.

To avoid the confounding effect of metabolic degradation, the stable mu-opioid peptide agonist [D-Arg2,Lys4]-dermorphin analogue (DALDA) was used to quantitate blood-brain barrier (BBB) permeability by intravenous injection and internal carotid artery perfusion techniques. With intravenous injection, the BBB permeability-surface area products for [3H]DALDA (0.84 +/- 0.13 microliters.min-1.g-1) and [14C]sucrose (0.39 +/- 0.05 microliters.min-1.g-1) correlated with the lipid solubility of the two molecules: the 1-octanol-Ringer partition coefficient for DALDA was approximately 2 log orders greater than that for sucrose. The brain delivery of [3H]DALDA at 30 min after intravenous administration was 0.019 +/- 0.002% of the injected dose per gram, and analgesia was induced with a 5-mg/kg dose administered systemically. In contrast to the result after intravenous injection, the BBB permeability-surface area product for DALDA estimated with the internal carotid artery perfusion technique was manyfold greater. This was due to nonspecific absorption of the peptide into the cerebral microvasculature, which precluded use of the capillary depletion technique to study transcytosis through the BBB after internal carotid artery perfusion. The present studies show that the brain delivery of a metabolically stable peptide, such as DALDA, is comparable to that for sucrose, correlates with lipid solubility, and is mediated by a nonsaturable mechanism, probably free diffusion.

Analgesics↗
PubMed1991

Retrosigmoidal approach to the posterior cranial fossa. An anatomical study.

An anatomical study was performed in order to obtain help for orientation regarding the retrosigmoid approach and its osteoclastic craniotomy. The insertions of the sternocleidomastoid, the splenius capitis, the longissimus capitis and the obliquus capitis superior muscles were measured. The relationships of the insertions to different landmarks were also ascertained (FHP, suprameatal spine). In 37 specimens 6 burrholes with a standardized relationship to the Frankfurt Horizontal Plane (FHP) and the external auditory meatus, were performed. Due to the results of the relationship between burrholes and the sigmoid and transverse sinuses it is possible to give an optimal position for the initial burrhole of the osteoclastic craniotomy. A burrhole performed according to the result of this study has a relatively small risk concerning iatrogenic bleeding from the sigmoid and transverse sinuses caused by the burrhead of the drill.

Cephalometry↗
PubMedDate not supplied

Manganese neurotoxicity: a review of clinical features, imaging and pathology.

Manganese intoxication can result in a syndrome of parkinsonism and dystonia. If these extrapyramidal findings are present, they are likely to be irreversible and even progress after termination of the exposure to manganese. Clinical features are usually sufficient to distinguish these patients from those with Parkinson's disease. The neurological syndrome does not respond to levodopa. Imaging of the brain may reveal MRI signal changes in the globus pallidus, striatum, and midbrain. Positron emission tomography reveals normal presynaptic and postsynaptic nigrostriatal dopaminergic function. The primary site of neurological damage has been shown by pathological studies to be the globus pallidus. The mechanism of toxicity is not clear.

Animals↗