Sweating In MS

A 10-year-old male with Multiple Sclerosis complained of excessive Sweating on the right side of the forehead and shoulder on relapse 3 months after the onset of Multiple Sclerosis.

Because the Neurologic Evaluation revealed no abnormalities in the SudoMotor function, it is likely that the HyperHidrosis resulted from a lesion in the central or PreGanglionic Sympathetic Nervous System.

Magnetic Resonance Imaging demonstrated a high-intensity lesion involving the left HypoThalamus on T₂-weighted imaging. Thus HypoThalamic involvement might be the reason for the HyperHidrosis in this patient.

A 49-year-old woman, with a two-year-history of Multiple Screlosis (MS), noticed Postural Dizziness, Intractable Hiccups and Vomiting.

On admission, she had mild Quadriparesis, Hypesthesia below the C5 level, and a Girdle Sensation at the T5 and L1 levels. A CSF examination showed slight increases in the protein level (48 mg/dl) and cell count (7/mm3). Brain MRI demonstrated no obvious lesion in the Medulla Oblongata.

The Head-Up-Tilting Test showed a decrease in the blood pressure from 105/63 mmHg to 70/55 mmHg. The pulse rate, however, increased from 57/min to 72/min. The Cold Pressure Test also revealed a mild impairement in her blood pressure response.

The R-R interval variation (coefficient of variation: CVRR) during normal breathing was 2.58 (normal: > 1.66). The Valsalva Ratio was 1.84 (normal: 1.4-2.0).

The Aschner Eye-Ball Pressure Test, the blood pressure response to the injection of Epinephrine, and the Sweating Response to the injection of Acetylcholine were all normal.

She was thus administered Domperidone and Chlorpromazine. Only Domperidone effectively improved the Nausea and Vomiting.

All symptoms, including Orthostatic Hypotension, Hiccups and Vomiting, disappeared about one month after admission. The remission of her symptoms was considered to reflect the natural course of MS.

The results of Autonomic Nervous System function tests and her clinical features suggest that an irritable lesion in the Medullary Tegmentum, including the Nucleus Tractus Solitarii, most likely caused her symptoms.

The above findings indicate that Autonomic symptoms, such as Orthstatic Hypotension, Hiccups and Vomiting, may sometimes be the only symptoms observed in a relapse of MS.

The aim of the study was ElectroPhysiologic assessment of Sudomotor Function and some aspects of CardioVascular System function in patients with Multiple Sclerosis and an attempt of referring assessed variables to duration of the disease and EDSS score.

The study included 24 patients with Clinically Definite, Relapsing/Remitting Multiple Sclerosis and 22 healthy, age-matched controls.

Autonomic functions were evaluated by means of clinical examination, Heart rate variability tests, measures of blood pressure in supine and standing position and Skin Sympathetic Response examination.

Clinical symptoms in patients with Multiple Sclerosis were scarce. ElectroPhysiologic tests showed no abnormalities in Heart rate variability and blood pressure response to standing in studied group.

The majority of patients presented with subclinical dysfunction of SudoMotor System, indicated by an abnormal Sympathetic Skin Response, which did not correlate with duration of the disease or EDSS score.

Sympathetic skin response examination proved to be a sensitive indicator of Autonomic disturbances in patients with Multiple Sclerosis.

Centrally and locally mediated Sympathetic VasoConstrictor Responses in skeletal muscle and subcutaneous tissue were studied in six patients with Definite Multiple Sclerosis and severely affected ThermoRegulatory Sweating.

The purpose of the study was to evaluate VasoMotor function in patients with pronounced ThermoRegulatory Dysfunction and to differentiate between locally and Centrally elicited VasoMotor Reflexes in two different tissues.

The method used, the 133-Xenon washout technique, makes such a distinction possible.

In spite of the severe Sweating disturbances, we found Centrally and locally mediated Sympathetic VasoMotor reflexes to be preserved in skeletal muscle and subcutaneous tissue.

The results support the view that SudoMotor and VasoMotor functions are independently controlled.

Previously described differences in Sympathetic VasoConstrictor Responses in skeletal muscle and subcutaneous tissue in several other Neurological Disorders are not present in patients with Multiple Sclerosis, based on our results.

Five patients with Clinically Definite Multiple Sclerosis are reported who presented with acute relapses associated with HypoThermia. Repeated episodes of HypoThermia were seen in four.

ThromboCytopenia was associated with the HypoThermia in four patients. Further investigation disclosed a tendency to chronic HypoThermia and suggested an altered ThermoRegulatory set point in one patient.

When MRI, Endocrine, and Autonomic studies failed to localize a lesion in the HypoThalamus, but subsequent necropsy showed HypoThalamic lesions.

In such patients a predisposition to altered ThermoRegulation may occur due to direct involvement of the HypoThalamus or from combined lesions affecting HypoThalamic outflow to the BrainStem and Spinal Cord.

We studied Sympathetic Skin Responses (SSRs) following Magnetic Stimulation of the neck in 40 normal subjects and 54 patients with Neurological Diseases and Active Sweat Gland Densities (ASGDs) at the foot induced by Pilocarpine in 39 patients.

SSRs at the hand following Magnetic Stimulation showed the lowest coefficients of variability of the latencies and amplitudes in eight consecutive responses compared with SSRs following other types of stimuli (Electrical and Auditory stimulation, and deep inspiration) in 12 normal subjects.

Fourteen of 38 patients with Neuropathies (37%) showed the presence of SSRs after Magnetic Stimulation, but not after Median Nerve stimulation.

Although SSRs to Magnetic Stimulation corresponded with those to Nerve stimulation in all patients with Multiple Sclerosis or Multiple System Atrophy.

These results suggest that the absence of SSRs after Nerve stimulation in patients with Neuropathies may be due to abnormalities of the Peripheral Sensory Afferent Fibers.

ASGDs significantly correlated with SSRs at the foot following Magnetic Stimulation, but not with those following nerve stimulation in patients with Neuropathies.

Magnetic Stimulation of the neck is the highly reproducible method of evoking SSRs because this technique is able to produce strong Sensory Afferent Inputs proximally.

Furthermore, SSRs following Magnetic Stimulation, little influenced by Sensory Afferent Fiber involvement, are very useful for evaluating the PostGanglionic Sympathetic function in patients with Neuropathies.

A 36-year-old woman had, since the age of 24, numerous episodes of Visual Loss and Spinal symptoms and signs at various levels, and was diagnosed as Multiple Sclerosis (MS).

CSF Myelin-Basic-Protein was increased. Neurological and ElectroPhysiological investigations suggested the Peripheral Nerve involvement. Sural Nerve biopsy performed about six years after the onset, revealed severe loss of both Myelinated and UnMyelinated Fibers.

Subsequently, Histamine Skin Reaction was defective in the lower limbs. Tests on SudoMotor and Pupillary functions indicated deficits of both Central and PostGanglionic Sympathetic Systems.

Though we could not detect causative factors for the Peripheral Nerve lesions, our patient appears to be the first documented case of MS associated with Axonal Degeneration of the Peripheral Somatic and Autonomic Nervous Systems.

Two patients with Multiple Sclerosis developed symptomatic Chronic Inflammatory DeMyelinating PolyNeuropathy with massive Spinal or Cranial Nerve hypertrophy revealed by neuroimaging.

Sural nerve biopsy in one showed only moderate DeMyelination, axonal loss, and onion-bulb formation, illustrating dichotomy between severe proximal and milder distal nerve involvement.

Patients with coexistent Central and Peripheral DeMyelination usually are symptomatic from dysfunction at one site or the other, but not from both. Our patients showed minimal response to Steroids, IntraVenous ImmunoGlobulin, or Azathioprine.

These cases suggest that the mechanism of disease in symptomatic Central and Peripheral DeMyelination may differ from that of disease in only one region, and that optimal therapy in this situation must be explored further.