oh sleeping on my back messes me up too. stupid walls keep getting in my way when i get up.
as far as gimpy handedness goes, i think my nerve conduction gets just as messed up when i'm out in the cold as it does when i sleep on my back.
couple of abstracts re normal nerves, demyelinated nerves:
Muscle Nerve. 1994 Mar;17(3):336-44.
Nerve conduction and temperature: necessary warming time.
Franssen H, Wieneke GH.
Rudolf Magnus Research School in the Neurosciences, Department of Clinical Neurophysiology, Utrecht, The Netherlands.
The purpose of this study was to estimate the time needed to warm an extremity prior to measuring nerve conduction. In 8 normal subjects tibial and sural nerve conduction variables were measured during cooling and warming of the leg in water of 18 degrees C and 36 degrees C, respectively. During cooling, nerve conduction velocity (NCV) decreased and distal motor latency (DML), duration, and area of the compound muscle action potentials (CMAP), and compound nerve action potentials (CNAP) increased. The reverse occurred during warming. During cooling or warming the change in these variables became progressively smaller with time. The time course could therefore be described by an exponential relation, the parameters of which were determined. On the basis of these data, correlations were calculated between the skin temperature at the start of the investigation and the warming time needed to obtain a good estimate of nerve conduction variables at 36 degrees C. The use of correction factors, instead of actual warming, yielded acceptable errors only for NCV and not for the other variables.
J Neuroophthalmol. 1995 Jun;15(2):70-8.
J Neuroophthalmol. 1995 Jun;15(2):63-9.
Visual evoked potentials during hyperthermia.
Saul RF, Hayat G, Selhorst JB.
Department of Neurology, Geisinger Medical Center, Danville, Pennsylvania, USA.
OBJECTIVES: We sought to evaluate the effect of hyperthermia (HT) on central conduction pathways by alterations in pattern visual evoked potentials (PVEPs) in normal and demyelinated optic nerves. MATERIALS AND METHODS: We studied PVEP peak latency and amplitudes in 10 normal subjects and six patients with demyelinating optic neuropathy before and during HT. RESULTS: In normal subjects, a mean rise in temperature of 2.5 degrees C resulted in a decrease in the second positive peak (P2) latency of 6.1 ms (p < 0.0001) and a slight decline in P2 amplitude of 1.16 muV (p < 0.009). These results were compared to those obtained from six patients with multiple sclerosis. These patients had a history of monocular optic neuritis; two patients had had bilateral optic neuritis, and one patient had not had involvement of the optic nerve. Average temperature elevations during PVEPs were 1.60 degrees C. PVEPs among these patients showed decrease in mean P2 latencies, except in patients with multiple sclerosis, who showed an increase in latency with 60 min check size in the left eyes. There was a consistent decline in P2 amplitudes. Loss of amplitude was greater among the six optic nerves of those patients having transient, mild losses in visual acuity during HT. Reductions in P2 amplitude were best explained by partial or complete conduction block. CONCLUSIONS: These changes in conduction time and amplitude during HT provide a neurophysiologic correlation to the well-known sensitivity of demyelinated optic nerves to elevated temperatures. They are also relevant to the monitoring of central pathways in the operative or intensive care setting. The demonstrated reversible loss of amplitudes also gives promise to therapeutic manipulation of impaired pathways by impeding the loss of current from denuded nerve fibers.