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Biomedical subjects

R Sandyk

Publications and source records attributed to R Sandyk.

At least 289 records · Page 16Linked to original sources
PubMed1987

Intracranial haemorrhage in a 26 year-old woman with idiopathic thrombocytopenic purpura.

Intracranial haemorrhage (ICH), a rare complication of idiopathic thrombocytopenic purpura (ITP), described only once previously in an adult, is usually fatal. We report a previously healthy 26 year old woman with chronic ITP in whom spontaneous ICH developed. The eventual favourable outcome in this case despite severe initial neurological deficit makes this case unusual. The importance of aggressive management in an ITP associated ICH is stressed and a plan for management is suggested.

Adult↗
PubMed1987

Baclofen in the treatment of post-amputation autonomous stump movements.

Baclofen at 20-40 mg/day was used to successfully treat two post-amputation patients who developed continuous complex involuntary movements of the proximal extremity. These autonomous movements were otherwise recalcitrant to therapy and were felt to arise from neural generators intrinsic to the spinal cord. Baclofen is known to be useful for spasticity of spinal etiology and now appears to be indicated for treatment of involuntary autonomous movements in post-amputation patients.

Amputation, Surgical↗
PubMed1987

Pain management after lower extremity amputation.

Phantom pain may occur in up to 85% of patients after limb amputation. Although the pathophysiology of postamputation phantom pain is not well understood, it seems to be produced by a complex multifactorial interaction between the peripheral, sympathetic, and central nervous systems. The theoretical aspects of this are reviewed. Management of phantom limb pain may be both medical and surgical. Among the pharmacological agents proved effective against phantom pain are beta-blockers, tricyclic antidepressants, and anticonvulsants. Surgical management includes peripheral nerve stimulation, thermocontrolled coagulation of the spinal cord, spinal cord stimulation, transcutaneous nerve stimulation, and stereotactic deep brain stimulation.

Adrenergic beta-Antagonists↗
PubMed1987

Opioid neuronal denervation in Gilles de la Tourette syndrome.

Increased striatal dopaminergic functions with heightened postsynaptic receptor sensitivity has been proposed to underlie the major clinical symptoms of Tourette's syndrome (TS). The beneficial response of the majority of TS patients to haloperidol supports the hyperdopaminergic pathophysiological concept of TS. However, in 5 recently encountered TS patients, haloperidol failed to ameliorate self-injurious behavior (SIB) while the opiate antagonist, naloxone, attenuated SIB, implicating deranged endorphinergic mechanisms in the pathophysiology of this disorder. Brain damage is commonly associated with partial neuronal denervation, denervation supersensitivity and neuronal habituation (Cannon's Law). While the motor tics of TS possibly reflect neuronal denervation of striatal dopaminergic neurons. SIB may represent opioid denervation with alterations in opioid receptor sensitivity possibly involving striato-limbic-hypothalamic circuits. The effect of naloxone on SIB in TS could thus be explained on the basis of a modulatory effect of this drug on opioid receptor sensitivity.

Brain↗
PubMed1987

The hypothalamus in Tourette's syndrome.

Although a recent report by Devinsky (1983) has suggested that dysfunction at a midbrain levels is most likely to underlie the major symptoms of Tourette's syndrome, several features of the disease including alterations in the severity of the disease during puberty and premenstrually, disorders of appetite, amelioration of tics with rise in body temperature, and sleep point to hypothalamic involvement in the pathophysiology of the disease.

Humans↗
PubMed1987

Clonidine in neuropsychiatric disorders: a review.

We describe the basic pharmacological principles underlying the activity of the alpha 2-adrenergic receptor agonist clonidine, including its interactions with the cholinergic, histaminergic, serotoninergic, endorphinergic and possibly dopaminergic systems. The use of clonidine for the therapy of various neuropsychiatric indications in which it appears to be beneficial is described. These conditions include migraine, Korsakoff's psychosis, Tourette's syndrome, withdrawal states, tardive dyskinesia, essential tremor, neuroleptic-induced akathisia, neurogenic bladder, idiopathic orthostatic hypotension, paroxysmal localised hyperhydrosis, diabetic neuropathy and stiff-man syndrome. The need for long term evaluation of this agent in some of these diseases is stressed.

Clonidine↗