Effects of carpal tunnel syndrome on adaptation of multi-digit forces to object texture

Objective

The ability to adapt digit forces to object properties requires both anticipatory and feedback-driven control mechanisms which can be disrupted in individuals with a compromised sensorimotor system. Carpal tunnel syndrome (CTS) is a median nerve compression neuropathy affecting sensory and motor function in a subset of digits in the hand. Our objective was to examine how CTS patients coordinate anticipatory and feedback-driven control for multi-digit grip force adaptation.

Methods

We asked CTS patients and healthy controls to grasp, lift, and hold an object with different textures.

Results

CTS patients effectively adapted their digit forces to changes in object texture, but produced excessive grip forces. CTS patients also produced larger peak force rate profiles with fewer modulations of normal force prior to lift onset than did controls and continued to increase grip force throughout the lift whereas forces were set at lift onset for the controls.

Conclusions

These findings suggest that CTS patients use less online sensory feedback for fine-tuning their grip forces, relying more on anticipatory control than do healthy controls.

Significance

These characteristics in force adaptation in CTS patients indicate impaired sensorimotor control which leads to excessive grip forces with the potential to further exacerbate their median nerve compression.     

Sonographic diagnosis of carpal tunnel syndrome--diagnostic value of the triangular cross-section sign

Background and purposeCarpal tunnel syndrome (CTS) is a common neuropathy resulting from compression of the median nerve at the carpal tunnel. Sonographic diagnosis of this condition relies on enlargement, flattening and/or demonstration of impaired mobility of the median nerve, as well as bowing or thickening of the flexor retinaculum. In most patients the cross-section of the median nerve at the level of the carpal tunnel has an oval or elliptical shape. We have noticed, however, that in a number of cases the cross-section of the median nerve at the inlet of the carpal canal was deformed, assuming a triangular shape. The purpose of this study was to assess the diagnostic value of the triangular median nerve cross-section sign.Material and methodsOne hundred and thirty-nine sonographic examinations in 76 patients with clinical signs of CTS, and 25 examinations in 14 healthy volunteers were performed. Standard electrodiagnostic studies were performed in all symptomatic patients.ResultsTriangular shape of the median nerve cross-section in the carpal canal was observed in 13/118 (11.0%) median nerves with abnormal result of the electrodiagnostic study, and in 2/21 (9.5%) cases with a normal electrodiagnostic examination result. No such deformation was seen in the control group.ConclusionsThe triangular cross-section sign has high specificity (0.90) and positive predictive value (0.87) in diagnosis of CTS.     

Migrant sensory neuritis--electrophysiological and pathological study]

Migrant sensory neuritis, which was first proposed by Wartenberg, is very uncommon and only a few case reports have ever been published. We described one case of migrant sensory neuritis and discussed the pathogenesis of this disease. A 44-year-old man noticed numbness in the lateral aspect of the dorsum of the left foot in February 1985. Physically, there was hypoesthesia in the region of left sural nerve with positive Tinel's sign. During the next 4 years, pain, tingling sensation or hypoesthesia appeared in the regions of the right superficial radial nerve, right axillary nerve, left intercostal nerve, left lateral plantar nerve, digital nerve of the right second digit, left saphenous nerve, right superficial peroneal nerve, left superficial radial nerve, bilateral ulnar nerves and bilateral median antebrachial cutaneous nerves one after another in a migrating fashion. Tinel's sign was also positive at the right superficial radial nerve. In some occasions, decreased deep tendon reflexes were observed, but there had been no muscle weakness. Some nerves showed complete recovery, but others showed persistent involvement. Some nerves were affected repeatedly. Laboratory examination failed to clarify underlying disease except for mild liver dysfunction. Electrophysiological study showed reduced amplitude of the sensory nerve action potential (SNAP) of right sural nerve, left ulnar nerve, right superficial radial nerve and digital branch of right median nerve with preserved sensory nerve conduction velocity. SNAP of left sural nerve was absent. These findings mean the cause of the sensory disturbance is axonal degeneration rather than segmental demyelination. There were no abnormalities in motor nerve conduction study.(ABSTRACT TRUNCATED AT 250 WORDS)     

Post-traumatic medial nerve injury due to a foreign body

A case of delayed injury to the median nerve by glass fragment is described. A median nerve palsy developed 3 years after a minor injury, totally forgotten by patient. A 34-year-old patient presented with a painful progressive median nerve lesion, with a Tinel sign just below elbow. Surgical exploration revealed a glass fragment in close proximity to median nerve. The foreign body was removed. Improvement was noted immediately, but the patient continues to have slight paresthesiae in the fingers 1 year later.     

Delayed radial nerve palsy following a humeral shaft fracture]

We reported a 24-year-old man with right radial nerve palsy. He had suffered from a right humeral shaft fracture approximately three years before. The fracture was treated with intramedullary nailing. Our radiograph of the right upper limb showed callus around the fracture site. A nerve conduction study revealed conduction block of the radial nerve at the lateral side of the callus. Tinel's sign was present in the median nerve at the medial side of the callus. Surgical exploration revealed that the radial nerve trunk was compressed at the callus site. The median nerve trunk was close to the callus. We decompressed radial nerve trunk, and the patient's neurological symptoms improved gradually after the operation. Delayed radial nerve palsy has been reported only rarely, whereas acute compression of the nerve sometimes occurs after humeral shaft fractures. Morever, the median nerve also was vulnerable to compression at the site of callus. These findings underscore the importance of taking into account the possibility of delayed compression neuropathy after humeral shaft fracture.     

Characterization of tests of functional recovery after median and ulnar nerve injury and repair in the rat forelimb

The majority of human peripheral nerve injuries occur in the upper limb but the majority of studies in the rat are performed in the hindlimb. The upper and lower limbs differ in dexterity and control by supraspinal systems, so an upper limb model is a better representation of the common form of human injury. The purpose of this study was to further develop a rat model involving lesions of the median and ulnar nerves. To produce different degrees of misdirection of axons following nerve repair, we studied nerve crush, cut and repair of the two nerves, and cut and repair with crossover. Assessment of functional recovery was performed using a battery of motor and sensory tests: the staircase test, which assesses skilled forepaw reaching; grip strength meter, which assesses grip strength; pawprint analysis, which assesses toe spread and print length; horizontal ladder, which assesses forepaw placement during skilled locomotion; modified Randall-Selitto device and electronic von Frey probes, which assess fine touch; and cold probes, which assess temperature sensation. All tests revealed deficits in forepaw function after nerve injury except the print length and modified Randall-Selitto device. The time course of functional recovery was observed over 15 weeks. The final degree of functional recovery achieved was related to the misdirection of axon regeneration. The tests that most clearly revealed the effects of axon misdirection on function were the skilled paw reaching and grip strength tests. The lesion model and functional tests that we have developed will be useful in testing therapeutic strategies for treating the consequences of inaccurate axon regeneration following peripheral nerve injury in humans.     

Cutaneous afferent activity in the median nerve during grasping in the primate

Neural activity was recorded from the median nerve of a monkey during grasping and lifting, using a chronically implanted cuff electrode. At the onset of lifting, there was an initial dynamic response during which the intensity of the neural signal increased rapidly. This neural response attained its peak value well before the displacement, the load force or the grip force. The time course and peak of the rectified, integrated neurogram were best correlated with the rate of change of grip force. The neural activity declined exponentially to a steady value following the initial peak. During steady holding the mean amplitude of the neurogram was best correlated with the mean grip force. At the end of the holding phase there was a short burst of neural activity as the monkey relaxed the grip force and released the object. During some blocks of trials pulse perturbations were applied to the object. When the monkey did not increase the grip force in advance of the perturbation, the perturbation produced a relatively large displacement of the object and a burst of neural activity whose onset coincided with the onset of displacement. When the monkey anticipated the perturbation by increasing the grip force during the holding period preceding the perturbation, the perturbation produced a relatively small displacement and relatively little increase in neural activity.     

Diagnostic tests in carpal tunnel syndrome

In a first series 100 patients underwent surgical treatment for carpal tunnel syndrome (CTS) after being tested by provocative tests for sensory disturbances preoperatively. In addition to the well-established tests like passive wrist flexion (Phalen's test) or wrist extension, active movement tests of the patient against resistance were investigated. Tests of active movement were introduced because of the high values of intraoperatively measured pressure at the median nerve, similar to those recorded with passive movements. All investigated provocative tests for sensory disturbances related to CTS, investigated by active and passive movements, were positive in 72% to 84% of patients. Average delay times for reaction of these provocative tests ranged between 15.7 and 19.5 s. Furthermore Tinel's sign showed a sensitivity of 64% and the flick sign one of 69%. The specificity of tests and signs for the CTS was assessed on a group of 50 surgically treated patients with cervical nerve root entrapment at the C5-C8 level. In this group and a second CTS group the most sensitive of each test in the first series (active and passive provocational movement), Tinel's sign and flick sign were investigated. By forming subgroups in both diseases we showed that the results of the total groups were not influenced by a possible double crush. We could demonstrate high sensitivities in cervical nerve root entrapment for Phalen's sign with 74% and for active thumb abduction with 68% and a medium sensitivity for Tinel's sign with 40%--thus implying low specificity for CTS. Only the flick sign turned out to be relatively specific for CTS--its sensitivity in cervical nerve root entrapment was around 26%--indicating its potential to function as a valid criterion for the differential diagnosis of CTS and cervical nerve root entrapment syndrome.     

"Tram-track" sign and "donut configuration" in Tolosa-Hunt syndrome]

We report unique MRI abnormalities seen in a patient with Tolosa-Hunt syndrome (THS). A 60-year-old woman was admitted for left eye symptoms, including periorbital pain, numbness around the left eyebrow, blurred vision, delayed light reflex and impairment of abduction. Laboratory studies were unremarkable except for elevated erythrocyte sedimentation rates. T1-weighted MRI showed a mass lesion in the left orbital apex. Fat-suppressed T2-weighted MRI showed a hyperintense parallel linear lesion on the left optic nerve and a ring lesion around it, producing the "tram-track" sign on the axial view and the "donut configuration" on the coronal view. A diagnosis of THS was made, and corticosteroid therapy was started. Symptoms were improved rapidly, and MRI abnormalities disappeared. Reevaluation of MRI which had been taken at the previous episode of the right eye symptoms two years before also showed the "tram-track" sign and the "donut configuration" on the right. These signs are easy to be recognized and well reflect the stage of the disease. They are thus useful for diagnosing THS and evaluating the effect of the treatment. One should pay attention not only to the cavernous sinus and orbital apex, but also to the optic nerve for the MRI diagnosis of THS.     

Complex regional pain syndrome secondary to leprosy

Introduction. Leprosy is a chronic infectious disease caused by Mycobacterium leprae affecting the skin and the nerves. Complex regional pain syndrome (CRPS/Sudeck's dystrophy) is a painful and disabling condition-a triad of autonomic, sensory, and motor symptoms disproportionate to the inciting event (inflammatory, infective, or traumatic nerve damage). Case. A 20-year-old male presented with continuous pain, aggravated by cold and emotions, loss of fine touch and temperature sensation, redness, swelling, along lateral aspect of left hand and forearm with weakness in the grip of 6 months' duration. There was a 5-year history of sensory loss only over left index finger that he ignored. Examination revealed abnormal sensory and autonomic functions along left radial and median nerve distribution that were confirmed by nerve conduction studies suggestive of mononeuritis multiplex. Radial cutaneous nerve biopsy was suggestive of leprosy. Magnetic resonance imaging and ultrasonography showed no compressive etiology; however, MRI showed involvement of brachial plexus. Antileprosy, anti-inflammatory drugs, and steroids were given in view of neuritis because of lepra reaction with supportive measures of physiotherapy, transcutaneous electrical nerve stimulation, to no avail. A surgical median nerve decompression also failed to relieve the pain. Temporary stellate ganglion block improved the pain scale. Thus, excluding all other causes, the final diagnosis was CRPS secondary to leprosy. There is only one reported case of CRPS with leprosy. Conclusion: Leprous neuropathy caused the nerve damage that lead to CRPS type 2. Very rarely leprosy can lead to CRPS. CRPS is a diagnosis of exclusion.     

A case of chronic inflammatory demyelinating polyradiculoneuropathy with orthostatic hypotension

A 27-year-old man was admitted to our hospital for his legs' numbness of subacute onset and discomfort while standing. No specific previous history was found and his family history was non-contributory. On admission, his general status was unremarkable except for arterial hypertension and mild tachycardia. Moderate impairment of superficial sensations and dysesthesia were noted in the distal extremities, tongue, oral cavity, and lips. Deep sensation was moderately impaired in the lower legs. Romberg sign was positive. He had mild weakness in the proximal muscles of the lower extremities. Hyporeflexia was noted in all extremities, but Achilles reflexes were absent. Pathologic reflexes were not noted. He fainted after two minute standing. On laboratory examination, serum IgM, C3, and C4 were mildly elevated. CSF protein level was prominently high without CSF pleocytosis. MCV was mildly decreased, and F wave conduction velocity was prominently decreased in the posterior tibial nerve, SCV was also mildly decreased in the right sural nerve. Needle electromyography showed mild neuropathic changes. Left sural nerve biopsy showed no abnormal finding in the myelinated and unmyelinated fibers. A 60 degree head-up tilting test caused a hypotensive attack, and Valsalva ratio was decreased. However, hand grip test and cold pressor test were normal. The response to noradrenaline infusion test and CVR-R were also normal. Muscle sympathetic activity (MSA) was recorded from the tibial nerve using a tungsten microelectrode (Iwase, et al.). His basic activity was higher and responsiveness was lower than age-matched normal controls. The regression line existed above the normal range.(ABSTRACT TRUNCATED AT 250 WORDS)     

Carpal tunnel syndrome with an unusual cause: a malignant nerve sheath tumor of the median nerve

We report on the follow-up of a patient who developed symptoms suggestive of carpal tunnel syndrome. Symptoms were however atypical with involvement of the nondominant hand and with selective, fascicular, electroneurographic changes. During the surgical decompression of the median nerve at the wrist a tumor was found, corresponding to an isolated malignant peripheral nerve sheath tumor (MPNST) of mild type. A course of local radiation therapy was completed, with no sign of recurrence, and a normalization of the serum level of neurone specific enolase.     

Moving objects with clumsy fingers: how predictive is grip force control in patients with impaired manual sensibility?

OBJECTIVE: Anticipatory grip force adjustments to movement-induced load fluctuations of a hand-held object suggest that motion planning is based on an internal forward model of both the external object properties and the dynamics of the own motor apparatus. However, the central nervous system also refers to real time sensory feedback from the grasping digits in order to achieve a highly economical coupling between grip force and the actual loading requirements. METHODS: We analyzed grip force control during vertical point-to-point arm movements with a hand-held instrumented object in 9 patients with moderately impaired tactile sensibility of the grasping digits due to chronic median nerve compression (n = 3), axonal (n = 3) and demyelinating sensory polyneuropathy (n = 3) in comparison to 9 healthy age- and sex-matched control subjects. Point-to-point arm movements started and ended with the object being held stationary at rest. Load force changes arose from inertial loads related to the movement. A maximum of load force occurred early in upward and near the end of downward movements. RESULTS: Compared to healthy controls, patients with impaired manual sensibility generated similar static grip forces during stationary holding of the object and similar force ratios between maximum grip and load force. These findings reflect effective grip force scaling in relation to the movement-induced loads despite reduced afferent feedback from the grasping digits. For both groups the maxima of grip and load force coincided very closely in time, indicating that the temporal regulation of the grip force profile with the load profile was processed with a similar high precision. In addition, linear regression analyses between grip and load forces during movement-related load increase and load decrease phases revealed a similar precise temporo-spatial coupling between grip and load forces for patients and controls. CONCLUSIONS: Our results suggest that the precise and anticipatory adjustment of the grip force profile to the load force profile arising from voluntary arm movements with a hand-held object is centrally mediated and less under sensory feedback control. As suggested by previous investigations, the efficient scaling of the grip force magnitude in relation to the movement-induced loads may be intact when deficits of tactile sensibility from the grasping fingers are moderate.     

Enhanced function in nerve-injured hands after contralateral deafferentation

To explore whether contralateral deafferentation by tourniquet-induced anaesthesia can improve function in a nerve-injured hand, we investigated 14 patients with median or ulnar nerve injuries at wrist level. Deafferentation of the contralateral forearm and hand resulted in significantly improved tactile discrimination, threshold for perception of touch in the injured nerve area and in the area corresponding to the intact nerve in the injured hand, and significantly increased grip strength. Improvements lasted at least 15 min. The results show that hand function after peripheral nerve injury can be temporarily enhanced by manipulation of the process of brain plasticity. Our results may have practical applications in the rehabilitation of peripheral nerve-injured patients.     

Clinical disease severity and axonal dysfunction in hereditary motor and sensory neuropathy Ia

Abstract Background Hereditary motor and sensory neuropathy type Ia (HMSN Ia) is known as a primarily demyelinating peripheral nerve disease. Evidence is accumulating that axonal involvement determines the course of the disease process. Methods Fifty-one patients were investigated. Physical disability and impairments were scored. Nerve conduction velocities (NCVs) were used as indirect measures for myelination status and compound muscle/sensory nerve action potential (CMAP/SNAP) amplitudes served as indirect measures for axonal function. Results Median age was 39 years (range 6–69).Muscle weakness and sensory dysfunction was more severe in the legs than in the arms and distally more than proximally. However, more than 40% of the patients had proximal muscle weakness in the legs. Three point grip was used as representative of combined distal arm muscle groups. CMAP amplitude was the most important independent variable in a multiple linear regression model (forward selection) to explain the relation between three point grip strength and four different features, i. e., CMAP amplitude of the abductor pollicis brevis, median nerve MNCV, gender, and duration of signs and symptoms. The severity of axonal dysfunction was nerve length-dependent and was related to the myelination status. The mild physical disability due to both muscle weakness and sensory dysfunction was also related to axonal dysfunction. Conclusions In HMSN Ia, clinical disease severity at the impairment and disability levels is related to the severity of axonal dysfunction. Our data support the hypothesis that the myelination status is one of the factors that determine the extent of axonal dysfunction later in life. Proximal weakness of the legs is encountered in a considerable proportion of our patients.     

Translation and validation of an instrument for evaluation of severity of symptoms and the functional status in carpal tunnel syndrome

The objective of the present study was to translate, to do cultural equivalence and validation of the Levine et al. (1993) or Boston Carpal Tunnel Questionnaire (BCTQ) to Portuguese. The BCTQ application to patients, selected by the question "What was the reason that brought you to look for a physician and that led him to ask this examination?" showed very good reproducibility. The validity was measured through the comparison of the severity symptoms scores (SSS) and the functional status scores (FSS) with the results of grip forces, Minnesota, two point discrimination, Semmes-Weinstein filaments perception and sensory conduction at the median nerve. The internal consistency was evaluated through Chronbach's alpha coefficient comparing the SSS and the FSS. The measuring properties were evaluated through paired t-test between pre and pos-surgical scores. Reproducibility, internal consistency, validation and measuring properties of the translated BCTQ were similar to those found by Levine et al. with the original version.     

The pressure angle of the median nerve as a new magnetic resonance imaging parameter for the evaluation of carpal tunnel

Objectives

The purpose of this study was to compare the MRI findings of the wrists of patients with carpal tunnel syndrome (CTS) and controls. We present a new MRI parameter, the pressure angle of the median nerve, in CTS patients.

Patients and methods

The study included 55 wrists, 36 of which were diagnosed with CTS and 19 healthy controls. All subjects underwent clinical, electrophysiological, and MRI evaluation. Clinical and electrophysiological findings were staged according to the degree of deficit. MRI parameters including median nerve diameter (MR1) and width (MR2) at the pisiform bone level; median nerve diameter (MR3) and width (MR4) at the hamate bone level; carpal arch width (MR5); carpal arch height (MR6); pressure angle of the median nerve (MR7); carpal tunnel diameter at the pisiform bone level (MR8); carpal tunnel diameter at the hamate bone level (MR9) and median nerve-flattening ratio were investigated. Eighteen operated wrists were evaluated 8 weeks after surgery. Correlation between the MRI parameters, EMG and clinical signs were evaluated.

Results

Among the 36 wrists with CTS, 5.6% were mild cases, 55.6% were moderate, and 38.9% were severe. Electromyography staging was as follows: 5.6% mild, 52.8% moderate, and 41.7% severe. A good correlation between the clinical and electrophysiological staging of the wrists with CTS was demonstrated (P = 0.0001). Median nerve width and carpal tunnel diameter at the pisiform bone level were found to be significantly increased whereas median nerve diameter at the hamate bone level and pressure angle of the median nerve (PAMN) were significantly lower in CTS group in comparison to controls. After surgery, median nerve diameter and width at the pisiform bone level decreased whereas median nerve diameter at the hamate bone level increased. In addition, carpal arch height and PAMN were also found to be significantly increased (P = 0.0001). The carpal tunnel diameter and median nerve-flattening ratio increased at the hamate bone level post-operatively (P = 0.0001) with no change at the pisiform bone level.

Conclusion

The pressure angle of the median nerve may prove useful in the assessment of idiopathic CTS, both before and after surgery.     

Median-ulnar nerve communications: electrophysiological demonstration of motor and sensory fibre cross-over

Summary In a 33-year-old female with carpal tunnel syndrome the presence of anomalous communications between median and ulnar nerves was electrophysiologically demonstrated in the forearm. Motor latencies from proximal and distal stimulation sites along the median nerve fibres to the abductor pollicis brevis were identical. Proximal latency increased after procaine infiltration of the ulnar nerve at the wrist. Normal latency to the abductor digiti minimi was obtained on stimulation of the median nerve at the elbow. Along the sensory fibres of the median nerve orthodromic conduction velocity was markedly slowed from digit III to the wrist and normal from the wrist to the elbow. On supramaximal stimulation of digit III a sensory response was also recorded from the ulnar nerve at the wrist. On stimulation of digit V a sensory potential was recorded from the median nerve at the elbow. This appears to be the first electrophysiological demonstration of an anomaly involving both the motor and sensory fibres of both the median and the ulnar nerves.

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Zusammenfassung Bei einer 33-jährigen Patientin mit einem Carpaltunnelsyndrom wurde das Vorhandensein einer abnormen Verbindung zwischen N. medianus und N. ulnaris am Vorderarm elektrophysiologisch nachgewiesen. Die motorische Latenzzeit vom Medianusstamm zum M. abductor pollicis brevis waren von proximalen und distalen Reizorten aus identisch. Die proximale Latenz nahm nach Procaine-Infiltration des Ulnarnerven am Handgelenk zu. Eine normale Latenz zum M. abductor digiti minimi wurde nach Stimulation des N. medianus am Ellbogen nachgewiesen.Die sensible orthodrome Leitgeschwindigkeit am Medianus war bei Reizung des Mittelfingers und Ableitung vom Handgelenk hochgradig verlangsamt, jedoch normal vom Handgelenk zum Ellbogen. Bei supramaximaler Reizung des Mittelfingers wurde auch vom Ulnarnerven am Handgelenk eine sensorische Antwort erzeugt. Bei Reizung des Kleinfingers wurde ein sensorisches Potential vom N. medianus am Ellenbogen abgeleitet.Unseres Wissens ist dies der erste Fall, in welchem elektrophysiologisch eine Anomalie sowohl der motorischen wie der sensiblen Fasern von Median- und Ulnarnerven nachgewiesen wurde.

     

Giant axonal neuropathy in two siblings: clinical histopathological findings

OBJECTIVE: Giant axonal neuropathy is a rare, severe autosomal-recessive neurologic disease affecting both the peripheral and the central nervous system. In this article, we describe a detailed clinicopathological report of two affected sibs from a consanguineous Turkish family. PATIENTS: The index patient was a 6.5-year-old girl. Her intellectual development was normal. At the age of 3, her parents noticed progressive lack of balance and deterioration of motor skills. On examination, she had paresis and sensory loss more marked distally. Her mental status was normal. Her older brother had similar findings. RESULTS: Electrophysiological studies of young patients showed decreased median and ulnar nerve conduction velocities, absent peroneal motor potential, absent sensory nerve potentials and an EMG suggesting a neurogenic pattern. MRI showed mild cerebral and cerebellar atrophy. The nerve biopsy showed moderate myelinated nerve fibres loss, several regenerative clusters and multiple giant axons. Focal demyelination, hypertrophic "onion pulp" changes and endoneural fibrosis were also seen. Immunohistochemically, neurofilament protein accumulation was detectable in giant axons. CONCLUSIONS: This consanguineous family with two affected siblings and healthy parents complies with autosomal-recessive inheritance in GAN. In the majority of reported GAN cases, CNS involvement is described early in the course of the disease, but these patients did not present any sign of CNS involvement. GAN is a rare genetic disease of childhood involving the central and peripheral nervous systems. The diagnosis is easy with clinical, electrophysiological, and histopathological features, if it has been done. Early diagnosis is important, because of possible prenatal diagnosis.     

HEPATIC NEUROPATHY

The peripheral nerve function was affected in 31 out of 34 patients with severe chronic hepatic failure, 20 of whom had a surgical portacaval shunt. Clinical findings were confined to the legs, an elevated vibratory perception threshold (VPT) on the big toe being the most common sign. However, the nerve function in the arm was also impaired. During ischaemia the rise in VPT (index finger) was delayed in 18 patients. An equivalent slowing of the sensory nerve conduction velocity was recorded in the digit-wrist and the wrist-elbow segments of the median nerve, accompanied by a reduction in amplitude and an increase in temporal dispersion of the action potentials. The sensory threshold for electrical stimuli (digit 3) was significantly raised. The frequency of neurological findings suggests that a peripheral nerve dysfunction is an integral part of the severe chronic hepatic failure syndrome. There was no relation to the routine liver function tests or to the galactose elimination capacity, a measure of the functioning liver mass. Neurological findings occurred with the same frequency in patients with and without chronic alcoholism or a diabetic glucose tolerance test. From the distribution of findings it is suggested that hepatic neuropathy results from a metabolic inhibition of the nerve axon membrane function.