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A 34-year-old woman with long-standing multiple sclerosis had a 2-year history and physical signs of myasthenia gravis. The edrophonium chloride (Tensilon) test was positive. Repetitive stimulation of the ulnar nerve at 3 Hz did not show evidence of myasthenic response; however, a single-fiber electromyography demonstrated evidence of neuromuscular block as seen in myasthenia gravis, which was reversed to normal after intravenously administered edrophonium. The patient improved on anticholinesterase medication. It is suggested that patients with multiple sclerosis who have unusual features such as in the patient reported here should be investigated for the presence of myasthenia gravis to ensure proper treatment.

Abstract:Disordered Cholinergic Neurotransmission and Dysautoregulation After Acute Cerebral Infarction• The possible role of displaced neurotransmitter acetylcholine (ACh) in dysautoregulation was examined after experimental regional cerebral infarction was produced by occluding the middle cerebral artery (MCA) in baboons. Regional cerebral blood flow (rCBF) was measured after intracarotid injection of 133 Xenon using the gamma camera. Autoregulation was tested with metaraminol or angiotensin infusion and the autoregulation index (A.I.) was calculated. Acetylcholinesterase (AChE) was measured in brain tissue of noninfarcted and infarcted hemispheres. Cerebral arteriovenous (A-V) differences for cholinesterase (ChE) were also measured. Regional dysautoregulation was found in infarcted gray matter and correlated with increased AChE levels in the same zones of cortex and basal ganglia. The time course of onset of dysautoregulation correlated with increased ChE uptake by the brain. Intravenous infusion of the cholinergic neurotransmitter blocker, scopolamine, restored autoregulation to the ischemic zones. Autoregulation appears to be a myogenic reflex, influenced by neurogenic and metabolic mechanisms. Additional Key Words cerebral infarctionacetylcholine cholinesterase autoregulation regional cerebral blood flow D Apart from the well-known cholinergic neuronal neurotransmitter systems occurring at synapses throughout the central and peripheral nervous system, whereby acetylcholine (ACh) is released from presynaptic vesicles and is inactivated by cholinesterase (ChE), it has been recently confirmed by histochemical methods that there is a rich cholinergic innervation of cerebral vessels accompanying their adrenergic nerves. Nevertheless, there is meager information concerning the functional significance of the cholinergic nerves in controlling cerebral blood flow (CBF).

SYNOPSISRegional cerebral blood flow (rCBF) was measured in baboons by intracarotid injection of 133Xe and a gamma camera after acute cerebral infarction was induced by occlusion of the middle cerebral artery (MCA). A steady state rCBF was measured four hours after MCA occlusion and was followed by bilateral ligation of the external carotid arteries (ECA). Subsequent rCBF measurements were obtained at 30, 60, and 120 minutes. After bilateral ECA ligation, flow in ischaemic and non-ischaemic areas was greatly enhanced and flow in the hyperaemic areas significantly reduced, presumably since they had provided collateral circulation to the ischaemic zone with a favourable redistribution.

Abstract:Regional Xe into the MCA were 15% to 20% lower than those obtained by intracarotid injection of 133 Xe. Possible explanations for these differences are discussed. During induced hypertension autoregulation in ischemic areas was abolished and paradoxical responses of LCBF and rMCAP to changes in arterial carbon dioxide tension (Paco' 2 ) were confirmed.