Thermoregulation is a vital function of the autonomic nervous system in response to cold and heat stress. Thermoregulatory physiology sustains health by keeping body core temperature within a degree or two of 37°C, which enables normal cellular function. Heat production and dissipation are dependent on a coordinated set of autonomic responses. The clinical detection of thermoregulatory impairment provides important diagnostic and localizing information in the evaluation of disorders that impair thermoregulatory pathways, including autonomic neuropathies and ganglionopathies. Failure of neural thermoregulatory mechanisms or exposure to extreme or sustained temperatures that overwhelm the body's thermoregulatory capacity can also result in potentially life-threatening departures from normothermia. Hypothermia, defined as a core temperature of 40.5°C, may present with sweating, flushing, tachycardia, fatigue, lightheadedness, headache, and paresthesia, progressing to weakness, muscle cramps, oliguria, nausea, agitation, hypotension, syncope, confusion, delirium, seizures, and coma. Mental status changes and core temperature distinguish potentially fatal heat stroke from heat exhaustion. Management requires the immediate reduction of core temperature. Ice water immersion has been shown to be superior to alternative cooling measures. Avoidance of thermal risk and early recognition of cold or heat stress are the cornerstones of preventive therapy.

Thermoregulatory disorders and illness related to heat and cold stress.

Acute necrotizing encephalopathy (ANE) is a rare but distinctive type of acute encephalopathy with global distribution. Occurrence of ANE is usually preceded by a virus-associated febrile illness and ensued by rapid deterioration. However, the causal relationship between viral infections and ANE and the exact pathogenesis of ANE remain unclear; both environmental and host factors might be involved. Most cases of ANE are sporadic and nonrecurrent, namely, isolated or sporadic ANE; however, few cases are recurrent and with familial episodes. The recurrent and familial forms of ANE were found to be incompletely autosomal-dominant. Further the missense mutations in the gene encoding the nuclear pore protein Ran Binding Protein 2 (RANBP2) were identified. Although the clinical course and the prognosis of ANE are diverse, the hallmark of neuroradiologic manifestation of ANE is multifocal symmetric brain lesions which are demonstrated by computed tomography (CT) or magnetic resonance imaging (MRI). The treatment of ANE is still under investigation. We summarize the up-to-date knowledge on ANE, with emphasis on prompt diagnosis and better treatment of this rare but fatal disease.

/pdf/acute-necrotizing-encephalopathy-an-underrecognized-2zerak0q9o.pdf

Acute necrotizing encephalopathy: an underrecognized clinicoradiologic disorder.

Topiramate (TPM; TOPAMAX®) is a broad-spectrum antiepileptic drug (AED) that is approved in many world markets for preventing or reducing the frequency of epileptic seizures (as monotherapy or adjunctive therapy), and for the prophylaxis of migraine. TPM, a sulfamate derivative of the naturally occurring sugar D-fructose, possesses several pharmacodynamic properties that may contribute to its clinically useful attributes, and to its observed adverse effects. The sulfamate moiety is essential, but not sufficient, for its pharmacodynamic properties. In this review, we discuss the known pharmacodynamic and pharmacokinetic properties of TPM, as well as its various clinically beneficial and adverse effects.

Molecular pharmacodynamics, clinical therapeutics, and pharmacokinetics of topiramate.

Neuroscientific developments have promulgated interest in developing efficacious medications for the treatment of substance dependence Previous pharmacological strategies that involve the use of relatively specific medications to alter corticomesolimbic dopaminergic neuronal activity--the critical pathway for expression of the reinforcing effects of abused drugs--have yielded modest efficacy in the treatment of alcohol dependence, and no medication has been established as a treatment for cocaine dependence Since corticomesolimbic dopaminergic neurons interact with other neurotransmitters that modulate the effects of dopamine in the nucleus accumbens, would it not be possible to control these dopaminergic effects more reliably with a medication that acts contemporaneously on more than one neuromodulator of dopaminergic function? Further, since the long-term use of either alcohol or cocaine results in neuronal adaptations as a result of sensitisation, would the chances of effective therapy not be bolstered by administering a medication that was also able to mitigate these chronic effects? Thus, a new conceptual approach is needed My proposal is that a medication--in this case topiramate--that principally potentiates inhibitory GABA(A) receptor-mediated input and antagonises excitatory glutamatergic afferents to the corticomesolimbic dopaminergic system should have therapeutic potential in treating either alcohol or cocaine dependence or perhaps both This is because the principal neurochemical effects of topiramate would not only serve to decrease the acute reinforcing effects of alcohol or cocaine, but might also facilitate cessation of their use following a period of long-term use by decreasing neuronal sensitisation This overview highlights the scientific concepts and clinical evidence for the development of topiramate in the treatment of alcohol dependence and introduces preliminary evidence to indicate that it might also have utility in treating cocaine dependence Finally, to place the material on topiramate in context, information has been included on the utility and development of other medications that modulate GABA- or glutamate-mediated neuronal systems for the treatment of alcohol or cocaine dependence

Recent advances in the development of treatments for alcohol and cocaine dependence: focus on topiramate and other modulators of GABA or glutamate function.

The human sweating response is subject to the influence of diverse classes of drugs. Some act centrally at the hypothalamus or at spinal thermoregulatory centres, while others act at sympathetic ganglia or at the eccrine-neuroeffector junction. Pharmacological disturbances of sweating have broad clinical implications. Drugs that induce hyperhidrosis, or sweating in excess of that needed to maintain thermoregulation, can cause patient discomfort and embarrassment, and include cholinesterase inhibitors, selective serotonin reuptake inhibitors, opioids and tricyclic antidepressants. Drugs that induce hypohidrosis, or deficient sweating, can increase the risk of heat exhaustion or heat stroke and include antimuscarinic anticholinergic agents, carbonic anhydrase inhibitors and tricyclic antidepressants. As acetylcholine is the principal neuroeccrine mediator, anhidrosis is one of the clinical hallmarks by which acute anticholinergic toxicity may be recognized. The symptom of dry mouth often accompanies the less apparent symptom of hypohidrosis because the muscarinic M3 acetylcholine receptor type predominates at both sweat and salivary glands. Management options include dose reduction, drug substitution or discontinuation. When compelling medical indications require continuation of a drug causing hyperhidrosis, the addition of a pharmacological agent to suppress sweating can help to reduce symptoms. When hypohidrotic drugs must be continued, deficient sweating can be managed by avoiding situations of heat stress and cooling the skin with externally applied water. The availability of clinical tests for the assessment of sudomotor dysfunction in neurological disease has enhanced recognition of the complex effects of drugs on sweating. Advances in the understanding of drug-induced anhidrosis have also enlarged the therapeutic repertoire of effective treatments for hyperhidrosis.

https://www.sweathelp.org/pdf/Drug-induced-hyperhidrosis-%20Cheshire.pdf

Drug-Induced Hyperhidrosis and Hypohidrosis : Incidence, Prevention and Management

A 6-year-old boy with partial complex seizures developed recurrent episodes of hyperthermia 2 months after topiramate was introduced into his antiepilepsy drug regimen Further investigation revealed that the febrile episodes were related to environmental temperature and physical activity A pilocarpine iontophoresis sweat test showed that the amount of sweat produced by the child was 5% that of age-matched controls Topiramate discontinuation resulted in the disappearance of febrile episodes and normalization of sweat quantity in repeat sweat testing Based on this observation and the previous data on zonisamide and isolated case reports on topiramate-related hyperthermia and the effect on sweat production, topiramate was suspected of causing oligohydrosis A pilot study was carried out involving 13 additional children and young adults (age range 1-37 years) receiving topiramate All patients were directly questioned regarding symptoms of decreased sweating and heat intolerance, went through a pilocarpine iontophoresis sweat test, and were compared with 14 age-matched controls who went through the sweat test for unrelated reasons Nine of the patients were found to have reduced sweat quantity on the pilocarpine iontophoresis sweat test (including index case) (mean 0089 g/30 minutes, SD 0082; age-matched control: mean 021 g/30 minutes, SD 006) Eight of them were children (below 16 years) However, only three patients revealed symptoms related to heat intolerance Topiramate is most likely responsible for decreased sweat production as detected by a pilocarpine iontophoresis sweat test The effect seems to be more significant in children than in adults There is a discrepancy between test results and clinical symptoms Interestingly, oligohydrosis was found to be a relatively common side effect of zonisamide Both zonisamide and topiramate share a carbonic anhydrase inhibitor activity The significance of oligohydrosis in hot climates should not be underestimated Its extent, the role of sweat test prediction, and clinical significance during topiramate treatment should be further estimated

Oligohydrosis and Hyperthermia: Pilot Study of a Novel Topiramate Adverse Effect

Acute necrotizing encephalopathy is a relatively new disease. The characteristic clinical findings are of febrile illness followed by rapid deterioration in mental status and seizures. The hallmark of the disease is multifocal bilateral symmetric lesions affecting the thalamus, hypothalamus, brainstem tegmentum, cerebral white matter, and cerebellum. The etiology is unknown, but immune-mediated mechanism was suggested. We present a 12-year-old previously healthy girl who developed increased sleepiness progressing to stupor and coma. Magnetic resonance imaging (MRI) of the brain showed the characteristic findings previously described in acute necrotizing encephalopathy. Her mental status improved dramatically with steroid treatment, and the MRI findings resolved completely within 6 months. Following the acute illness, she developed a complex neuropsychiatric disorder consistent with basal ganglia syndrome.

Acute necrotizing encephalopathy presenting as a basal ganglia syndrome.

https://www.pedneur.com/article/S0887-8994(01)00271-5/pdf

Acute onset of infantile spinal muscular atrophy

Two patients with acute generalized weakness and areflexia are presented. The electrophysiologic studies in both revealed evidence of decreased conduction velocity and mixed axonal and demyelinating neuropathy, suggestive of the diagnosis of Guillain-Barre syndrome. The young ages of the patients and their failure to respond to immunoglobulin therapy were the major clues to the final diagnosis of spinal muscular atrophy type I. Blood for DNA study revealed homozygous deletion mutation in exons 7 and 8 of the survival motor neuron gene. This diagnosis should be considered in every child under 1 year of age who presents with acute weakness because Guillain-Barre syndrome in this age group is rare.

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Oligohydrosis and Hyperthermia: Pilot Study of a Novel Topiramate Adverse Effect

Acute necrotizing encephalopathy presenting as a basal ganglia syndrome.

Acute onset of infantile spinal muscular atrophy

Acute onset of infantile spinal muscular atrophy