scholarly journals Some Observations on Tick Paralysis in Marmots

1960 ◽  
Vol 37 (2) ◽  
pp. 355-362
Author(s):  
PATRICIA EMMONS ◽  
H. McLENNAN

1. Observations have been made on marmots paralysed by the attachment of the ixodid tick Dermacentor andersoni Stiles. 2. Acetylcholine synthesis by excised tissues from paralysed animals is unaffected. 3. Conduction in both motor and sensory nerve fibres is markedly reduced. It is likely also that the excitability of neurones of the spinal cord is diminished. 4. There are changes in the electrocardiogram suggestive of a slowed rate of auricular and ventricular depolarization and repolarization.

1991 ◽  
Vol 16 (5) ◽  
pp. 477-482 ◽  
Author(s):  
T. CARLSTEDT

This review summarises studies aiming at a surgical treatment of spinal nerve root avulsions from the spinal cord in brachial plexus lesions. After dorsal root injury, regrowth of nerve fibres into the spinal cord occurs only in the immature animal. After ventral root avulsion and subsequent implantation into the spinal cord, neuroanatomical and neurophysiological data show that motoneurons are capable of producing new axons which enter the implanted root. Intra-neuronal physiological experiments demonstrate that new axons can conduct action potentials and elicit muscle responses. The neurons are reconnected in segmental spinal cord activity and respond to impulses in sensory nerve fibres. In primate experiments, implantation of avulsed ventral roots in the brachial plexus resulted in functional restitution. These studies indicate the possibility of surgical treatment of ventral root avulsion injuries in brachial plexus lesions in humans.


1957 ◽  
Vol 89 (1) ◽  
pp. 1-5 ◽  
Author(s):  
J. D. Gregson

Tick paralysis continues to be one of the most baffling and fascinating tickborne diseases in Canada. It was first reported in this country by Todd in 1912. Since then about 250 human cases, including 28 deaths, have been recorded from British Columbia. Outbreaks in cattle have affected up to 400 animals at a time, with losses in a herd as high as 65 head. Although the disease is most common in the Pacific northwest, where it is caused by the Rocky Mountain wood tick, Dermacentor andersoni Stiles, it has lately been reported as far south as Florida and has been produced by Dermacentor variabilis Say, Amblyomma maculatum Koch, and A. americanum (L.) (Gregson, 1953). The symptoms include a gradual ascending symmetrical flaccid paralysis. Apparently only man, sheep, cattle, dogs, and buffalo (one known instance) are susceptible, but even these may not necessarily be paralysed.


Neuroreport ◽  
1996 ◽  
Vol 7 (8) ◽  
pp. 1341-1342
Author(s):  
M. Riedl ◽  
S. Shuster ◽  
L. Vulchanova ◽  
J. Wang ◽  
H. Loh ◽  
...  

1967 ◽  
Vol 46 (1) ◽  
pp. 63-84
Author(s):  
K. M. CHAPMAN ◽  
J. H. PANKHURST

1. Conduction velocities of individual afferent nerve fibres from tactile spines and proprioceptive campaniform sensilla have been measured in situ over the temperature range 5-42° C., in leg preparations of the cockroach Periplaneta americana. 2. Conduction velocities at 20° C. (u20) averaged 3.3±1.4 m./sec., ranging from 1.6 to 11.0 m./sec. 3. Temperature coefficients, expressed as Q10 for the interval 20-30° C., averaged 1.7±0.24, ranging from 1.3 to 2.6. 4. The length of the propagated disturbance is about 2-3 mm., and is nearly temperature-independent. 5. Fibre diameters, estimated from conduction velocity, must be about 10 µ. 6. There is no correlation between conduction velocity and distance from the sensillum to the thoracic ganglion. Conduction delays in fibres conducting within one standard deviation of mean u20 range from about 2 to 15 msec., from the most proximal to the most distal tactile spines. 7. The effect of conduction delay on temporal and spatial sensory encoding is probably unimportant from a behavioural point of view. It contributes a factor of the form exp(-sd/u) to the sensory transfer function, and may be appreciable at upper physiological frequencies of impulse frequency modulation.


1963 ◽  
Vol 26 (6) ◽  
pp. 528-534 ◽  
Author(s):  
J. T. Hughes ◽  
B. Brownell
Keyword(s):  

1986 ◽  
Vol 11 (1) ◽  
pp. 125-130
Author(s):  
M. SAKURAI

Sympathetic nerve fibres innervating the sweat glands in the skin are known to accompany sensory nerve fibres closely. Examination of sudorific function, therefore, is a useful aid in making a diagnosis of severed peripheral nerve and also provides valuable information on nerve function in the recovery stage following injury and surgery such as neurorrhaphy. Among the many methods which have been used clinically, the one employing bromphenol blue is thought to be the most simple and accurate.


The demonstration of depolarization-induced release of substance P, Met- and Leu-enkephalin, somatostatin, neurotensin, vasoactive intestinal polypeptide and cholecystokinin-like material from various regions of rat brain in vitro supports the hypothesis that these and other neuropeptides may act as neurotransmitters. In each case the stimulusevoked release, but not the basal release, of peptide was dependent on the presence of calcium ions in the external medium. The stimulus-evoked release of substance P from nerve terminals in rat substantia nigra may be regulated by presynaptic γ -aminobutyric acid (GABA) receptors. The possible existence of presynaptic opiate receptors on substance P-containing sensory nerve terminals may offer an explanation for the analgesic effects of opiates at spinal cord level, and for the existence of enkephalin neurons in substantia gelatinosa. Capsaicin releases substance P from spinal cord nerve terminals and may impair their function, while having no effect on substance P neurons in supraspinal regions. The possibility of cosecretion of peptide and amine products from the same cells is discussed.


2007 ◽  
Vol 81 (12) ◽  
pp. 6605-6613 ◽  
Author(s):  
Andrea S. Bertke ◽  
Amita Patel ◽  
Philip R. Krause

ABSTRACT Herpes simplex virus (HSV) establishes latency in sensory nerve ganglia during acute infection and may later periodically reactivate to cause recurrent disease. HSV type 1 (HSV-1) reactivates more efficiently than HSV-2 from trigeminal ganglia while HSV-2 reactivates more efficiently than HSV-1 from lumbosacral dorsal root ganglia (DRG) to cause recurrent orofacial and genital herpes, respectively. In a previous study, a chimeric HSV-2 that expressed the latency-associated transcript (LAT) from HSV-1 reactivated similarly to wild-type HSV-1, suggesting that the LAT influences the type-specific reactivation phenotype of HSV-2. To further define the LAT region essential for type-specific reactivation, we constructed additional chimeric HSV-2 viruses by replacing the HSV-2 LAT promoter (HSV2-LAT-P1) or 2.5 kb of the HSV-2 LAT sequence (HSV2-LAT-S1) with the corresponding regions from HSV-1. HSV2-LAT-S1 was impaired for reactivation in the guinea pig genital model, while its rescuant and HSV2-LAT-P1 reactivated with a wild-type HSV-2 phenotype. Moreover, recurrences of HSV-2-LAT-S1 were frequently fatal, in contrast to the relatively mild recurrences of the other viruses. During recurrences, HSV2-LAT-S1 DNA increased more in the sacral cord compared to its rescuant or HSV-2. Thus, the LAT sequence region, not the LAT promoter region, provides essential elements for type-specific reactivation of HSV-2 and also plays a role in viral neurotropism. HSV-1 DNA, as quantified by real-time PCR, was more abundant in the lumbar spinal cord, while HSV-2 DNA was more abundant in the sacral spinal cord, which may provide insights into the mechanism for type-specific reactivation and different patterns of central nervous system infection of HSV-1 and HSV-2.


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