ABSTRACT
A 47-year-old woman developed acute Guillain-Barré-syndrome (GBS) within one day, presenting tetraparesis (muscle strength 1/5 for the upper and 2/5 for the lower extremities) and respiratory failure. On day 5 a cardiac pacemaker was necessary due to severe bradycardia. Electrophysiological studies were performed on days 2, 3, 5, 6, 8, 12, 15, 30 and 40. Our initial findings revealed normal motor conduction velocities and normal spinal motor evoked potentials. However, neither F-waves nor cortical motor evoked potentials could be registered from the upper or lower extremities. The motor conduction of the median nerve remained normal until day 6. The compound motor action potential declined thereafter and disappeared by day 12, indicating axonal degeneration. No axonal degeneration occurred in the lower extremities. The cervical or lumbar magnetic stimulation excites nerve roots at the level of the foramen intervertebrale. Thus, our findings suggest a conduction block between the foramen intervertebrale and the point where the nerve roots enter the spinal cord.
Subject(s)
Demyelinating Diseases/diagnosis , Electromagnetic Fields , Motor Neurons/physiology , Polyradiculoneuropathy/diagnosis , Spinal Nerve Roots/physiopathology , Synaptic Transmission/physiology , Afferent Pathways/physiopathology , Cerebral Cortex/physiopathology , Demyelinating Diseases/physiopathology , Evoked Potentials, Motor/physiology , Female , Humans , Median Nerve/physiopathology , Middle Aged , Polyradiculoneuropathy/physiopathology , Reaction Time/physiology , Retrograde Degeneration/diagnosis , Retrograde Degeneration/physiopathology , Tibial Nerve/physiopathologyABSTRACT
A procedure to make optical quality thin films of Zn(x)Cd(1-x)Te by use ofvacuum evaporation of the ternary compound has been developed. Thestarting point was the preparation of the compound that was then usedas the source in a simple vacuum evaporation system. Thecharacteristics of a film containing 85% ZnTe (x =0.85) are presented. Electron microscope, atomic forcemicroscope, x-ray and optical spectral measurements were made. Theindex of refraction was determined at room temperature fromtransmittance measurements in the range of from 580 to 800 nm and wasfound to agree within 1% with values found by others for singlecrystals. We did this by assuming a Sellmeier equation and a knownindex of refraction at infinite wavelength. The calculation alsoyielded the roughness of the film.
ABSTRACT
Cerebral involvement is typical for thrombotic microangiopathies like haemolytic uremic syndrome (HUS) and thrombotic-thrombopenic purpura (Moschcowitz disease or TTP). Symptoms are irritation, restless behaviour, disorientation, disturbance of consciousness, seizures, and focal neurological deficits. The lack of typical imaging changes or pathological observations may explain the unknown pathophysiological cascade leading to the neurological symptoms. We describe the development of HUS/ TTP in a 52-year-old woman after acute pneumonia caused by Diplococcus pneumoniae. The patient showed an increasing psycho-organic syndrome with disorientation, followed by severe loss of consciousness and coma. Initially, computed tomography showed slight diffuse brain oedema, which was not found in later follow-up images. Magnetic resonance imaging was normal. The TCD examination revealed general velocity increases and vasospasms (especially MCA, ACA and PCA bilateral and BA). The reduction in blood flow velocities in the basal arteries was accompanied by a marked clinical improvement. The development of vasospasms may be an explanation for the neurological deficits in HUS/TTP. The origin of the vasospasms may be found in disturbed prostacyclin production, increased serotonin or platelet factor IV release, and leucocyte activation with consecutive endothelial damage.
Subject(s)
Brain Edema/physiopathology , Coma/physiopathology , Hemolytic-Uremic Syndrome/physiopathology , Purpura, Thrombotic Thrombocytopenic/physiopathology , Blood Flow Velocity/physiology , Brain/blood supply , Brain Edema/diagnosis , Female , Hemolytic-Uremic Syndrome/diagnosis , Humans , Ischemic Attack, Transient/diagnosis , Ischemic Attack, Transient/physiopathology , Middle Aged , Neurologic Examination , Purpura, Thrombotic Thrombocytopenic/diagnosis , Tomography, X-Ray Computed , Ultrasonography, Doppler, TranscranialABSTRACT
Salicylates increase the risk of hemorrhage. An ischemic brain infarct has not previously been described following intoxication with salicylates. Case report. A 58-year-old comatose patient was admitted with symptoms of a basilar artery thrombosis. A diagnostic angiography was impossible because laboratory results showed a prothrombin time (Quick) of 9% and a toxic salicylate level of 528 mg/l. During the next few days CCT and MRI scans revealed ischemic infarctions within the brain stem. Discussion. Salicylates can induce hemorrhage both by inhibiting platelet aggregation and - especially in higher doses - by vitamin K antagonism, leading to severe coagulopathy. The occurrence of an ischemic infarction, as presented in this case report, can be explained by a reduction of the vitamin K-dependent protein C level.
Subject(s)
Aspirin/poisoning , Brain Stem/blood supply , Cerebral Infarction/chemically induced , Drug Overdose/complications , Basilar Artery/diagnostic imaging , Blood Coagulation Tests , Cerebral Angiography/drug effects , Cerebral Infarction/diagnostic imaging , Dose-Response Relationship, Drug , Humans , Intracranial Embolism and Thrombosis/chemically induced , Intracranial Embolism and Thrombosis/diagnostic imaging , Male , Middle Aged , Neurologic Examination/drug effectsABSTRACT
AIM: We treated 24 patients suffering from an acute ischemic stroke of the middle cerebral artery, with a hypervolemic hemodilution combined with dopamine/dobutamine. METHOD: The influence of blood pressure and cardiac output on the blood flow velocity in the middle cerebral artery was measured using transcranial Doppler sonography (TCD). RESULTS: Under the hypervolemic hemodilution supported with dopamine/dobutamine a dosage-dependent increase of 12% in blood pressure and a 53% increase in cardiac output was observed. In the affected hemisphere, flow velocity was one fourth lower (significance p < 0.05) than in the unaffected hemisphere. With therapy, the systolic flow velocity was increased in the unaffected hemisphere by 27%, on the side of the lesion only 11%. Mean flow velocity remained nearly constant. The pulsatility index (PI) increased simultaneously by 46% in the affected and 47% in the unaffected hemisphere. CONCLUSION: Similar effects on TCD-flow velocity and PI under comparable slight increases in blood pressure are not known. The increase in cerebrovascular resistance can be ascribed to a counter-regulation of the cerebral autoregulation, triggered by an increase of cardiac output.
