PubMed · 7020848
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K E Britton. 1980. Dynamic radionuclide imaging.. https://doi.org/10.1093/oxfordjournals.bmb.a071644
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Difficulties in location of transcranial ultrasound (US) windows and blood flow in cerebral vessels, and unambiguous detection of microemboli, have limited expansion of transcranial Doppler US. We developed a new transcranial Doppler modality, power M-mode Doppler (PMD), for addressing these issues. A 2-MHz digital Doppler (Spencer Technologies TCD100M) having 33 sample gates placed with 2-mm spacing was configured to display Doppler signal power, colored red and blue for directionality, in an M-mode format. The spectrogram from a user-selected depth was displayed simultaneously. This system was then explored on healthy subjects and patients presenting with varying cerebrovascular pathology. PMD facilitated window location and alignment of the US beam to view blood flow from multiple vessels simultaneously, without sound or spectral clues. Microemboli appeared as characteristic sloping high-power tracks in the PMD image. Power M-mode Doppler is a new paradigm facilitating vessel location, diagnosis, monitoring and microembolus detection.
Both dopaminergic neurotransmission and prefrontal cortex (PFC) function are known to be abnormal in schizophrenia. To test the hypothesis that these phenomena are related, we measured presynaptic dopaminergic function simultaneously with regional cerebral blood flow during the Wisconsin Card Sorting Test (WCST) and a control task in unmedicated schizophrenic subjects and matched controls. We show that the dopaminergic uptake constant Ki in the striatum was significantly higher for patients than for controls. Patients had significantly less WCST-related activation in PFC. The two parameters were strongly linked in patients, but not controls. The tight within-patient coupling of these values, with decreased PFC activation predicting exaggerated striatal 6-fluorodopa uptake, supports the hypothesis that prefrontal cortex dysfunction may lead to dopaminergic transmission abnormalities.
Intracranial hypertension develops from the initial cerebral effect of increased intracranial pressure and becomes symptomatical; then it acquires its individuality, surpassing the initial disease. The intracranial hypertension syndrome corresponds to the stage at which the increases in intracranial pressure (ICP) can be compensated and the ICH disease is in its acute form, equivalent to a decompensated ICH syndrome. Based on the etiopathogenesis of intracranial hypertension, a new classification is proposed: parenchymatous intracranial hypertension with an intrinsic cerebral cause; vascular intracranial hypertension, which has its etiology in disorders of the cerebral blood circulation; and essential or idiopathic intracranial hypertension, the former pseudotumor cerebri, an incomplete ICH syndrome. A synergetical pattern of the ICH is based on the relation between ICP and the period of high-pressure action: the critical pressure--time fluctuation causes the autoregulation of the cerebral blood flow to decrease or determines the brain herniation. The decompensation is a state of instability and appears when the intrinsic ratio of pressure--time fluctuation is changed: the high ICP lasts longer than the corresponding normal ICP, or the ICP is higher than the one that normally lasts the same period of time.