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Ataxia Induced by Small Amounts of Alcohol

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Ataxia Induced by Small Amounts of Alcohol 370 J Neurol Neurosurg Psychiatry 1998;65:370–373 J Neurol Neurosurg Psychiatry: first published as 10.1136/jnnp.65.3.370 on 1 September 1998. Downloaded from SHORT REPORT Ataxia induced by small amounts of alcohol F Setta, J Jacquy, J Hildebrand, M-U Manto Abstract following blood tests were normal: sedimenta- A patient is described who exhibited tion rate, glucose concentration, liver function cerebellar ataxia after drinking small tests, ammonia concentration, and red blood amounts of alcohol. Intake of 5 g alcohol cell transketolase (an index of thiamine nutri- induced a gaze evoked nystagmus, a scan- tional status4), vitamin E concentration. Inves- ning speech, a body sway after eye closure, tigations for a cardiomyopathy or an occult and bilateral postural leg tremor. Kin- malignancy were negative. Motor and sensory ematic and EMG analysis of fast wrist nerve conduction velocities in his lower limbs movements showed normal movements were also normal. He was given thiamine (600 before and marked hypermetria after mg/day) for 5 months with no eVect on the alcohol intake. Dysmetria was due to alcohol induced ataxia. abnormal programming of antagonist We examined this patient for the first time in muscle activity. 1997. He wanted to drink wine occasionally. (J Neurol Neurosurg Psychiatry 1998;65:370–373) There was no family history of neurological disease or enhanced susceptibility to alcohol Keywords: alcohol; cerebellum; hypermetria intake (his father and his two brothers drank from 10 to 50 g alcohol a day for more than 10 years without complaints). General physical Alcohol is a cause of late cortical cerebellar copyright. degeneration of the anterior lobe.1–3 These examination was unremarkable. There was no patients typically exhibit ataxia of the lower postural hypotension. Neurological examin- limbs, ataxia of gait, and trunk instability. Less ation showed normal mental status (mini men- frequent clinical findings include nystagmus, tal state examination (MMSE) 29/30). There dysarthria and upper limb incoordination.23 was no scanning speech, and finger-to-nose The neuropathological changes involve in par- test, fine finger movements, alternate move- ticular Purkinje cells at the level of the anterior ments of the hands, heel-to-knee test, Romb- and superior vermis, and paravermal parts of erg’s test, and tandem gait were all normal. the anterior lobe in more advanced cases.1 It Strength and careful sensory examination were has been shown that alcoholic patients exhibit- unremarkable. Tendon reflexes were brisk and ing cerebellar ataxia do not have higher alcohol plantar reflexes were flexor. The following consumption than non-ataxic alcoholic pa- blood studies were normal: blood cell count, http://jnnp.bmj.com/ Clinica Neurologica II, renal and liver function tests, albumin concen- Università La tients, suggesting that alcohol induced cerebel- Sapienza, Roma, Italia lar degeneration might be due to an idiosyn- tration, lipids, uricaemia, antinuclear antibod- F Setta cratic sensitivity to alcohol.4 We report on a ies, concentrations of vitamins B12 and folic patient with a normal neurological examin- acid, and thyroid function tests. No alcohol was Service de Neurologie, ation who showed a high vulnerability to small detected in his blood. Sensory evoked poten- CHU-Charleroi, doses of alcohol. Small quantities of alcohol tials (all four limbs), auditory evoked poten- Belgique tials, motor evoked potentials in the upper J Jacquy induced a cerebellar syndrome with character- istics reminiscent of a cerebellar cortical limbs, motor and sensory conduction velocities on September 24, 2021 by guest. Protected Service de Neurologie, atrophy of the anterior lobe. in the upper and lower limbs, and EEG were all Hôpital Erasme-ULB, within the normal range. Brain CT, brain MRI, Bruxelles, Belgique and single photon emission computed tomog- J Hildebrand Case report raphy (99mTc-HMPAO) were normal. Brain M-U Manto This 46 year old right handed man noted that, PET was not performed. Correspondence to: since the age of 15 years, small doses of alcohol With informed consent, we tested the effects Dr Mario-Ubaldo Manto, (about 200 ml beer or wine) induced clumsi- of 5 g alcohol given orally on neurological Service de Neurologie, ness in his legs and arms for 3 to 6 hours. He examination (20 minutes after alcohol intake) Fonds National de la Recherche Scientifique, had no history suggesting a subclinical cer- and on fast wrist flexion movements (30 Hôpital Erasme-ULB, 808 ebellar dysfunction after a previous disorder minutes after alcohol intake) in a control group Route de Lennik, 1070 such as a cerebellitis. From the age of 25 to 35, of five right handed healthy men (mean age 42 Bruxelles, Belgium. Telephone 0032 2 555 67 47; he used to drink about 10 to 20 g alcohol a day. (SD 5) years) and in our patient. In the control fax 0032 2 555 39 42. He subsequently stopped alcohol consump- group, this small dose of alcohol did not modify tion because of gait and speech diYculties the results of neurological examination. By Received 13 August 1997 after alcohol intake. In 1996, he sought medi- contrast, in our patient, movements in his and in final revised form 19 February 1998 cal advice in another department. upper limbs were irregular after alcohol Accepted 24 February 1998 Neurological examination was normal. The consumption, and we found a gaze evoked nys- EVects of alcohol on fast wrist movements 371 J Neurol Neurosurg Psychiatry: first published as 10.1136/jnnp.65.3.370 on 1 September 1998. Downloaded from copyright. http://jnnp.bmj.com/ (A) Kinematic features of fast and accurate right wrist flexions performed by the patient before (left part) and after alcohol intake (right part). Each panel corresponds to the superimposition of the individual records of position for 12 flexion movements. The aimed target is located at 15° from the start position. (B) Electromyographic features of fast flexions for right wrist before and after alcohol intake in our patient. Superimposition of the rectified and averaged agonist EMG activities (EMG AGO; top panel) and of the rectified and averaged antagonist EMG activities (EMG ANTA;bottom panel), before (thin traces) and after alcohol consumption (thick traces). The number of wrist flexions is 12. on September 24, 2021 by guest. Protected tagmus and a mild scanning speech. Romberg’s identical. The patient and healthy subjects test showed marked anterior and posterior were comfortably seated with the forearm oscillations after eye closure. A low frequency wrapped on to the arm of an armchair. Palm bilateral postural leg tremor with a waxing and and fingers were wrapped on to a rigid light waning amplitude and which predominated on plate to avoid unwanted rotations of joints the right side was present. Tandem gait other than the wrist. Computerised motion required one aid. Strength and sensory analysis in three dimensions was made with a examination were normal, tendon reflexes were Selspot II system (Selcom, Sweden). One unchanged, and plantar reflexes remained infrared light emitting diode was attached to flexor. the forefinger. Sampling rate was 300/s. Veloc- We analysed kinematics and EMG indices of ity curves were obtained after digital diVeren- agonist (flexor carpi radialis) and antagonist tiation of the position signal. The aimed target (extensor carpi radialis) activities associated was located 15° away from the starting position with fast wrist flexion movements before (basal and we recorded 12 movements in both condi- condition) and after intake of alcohol, using a tions. The EMG signals were amplified, filtered method previously described.5 Experimental (2000×; 30–8000 Hz), full wave rectified, and conditions before and after alcohol intake were averaged. 372 Setta, Jacquy, Hildebrand, et al J Neurol Neurosurg Psychiatry: first published as 10.1136/jnnp.65.3.370 on 1 September 1998. Downloaded from Results that rapid voluntary movements were hyper- In the control group, mean movement ampli- metric due to the inability to generate a tude was 15.3 (SD 0.9)° before and was 14.9 suYcient rate of rise of the antagonist activity. (SD 1.0)° after alcohol intake (Student’s t test; Such a cerebellar hypermetria associated with p=0.61). The mean peak velocity was 597 (SD an inability to develop a normal rate of rise of 35)°/s before and 588 (SD 42)°/s after alcohol the antagonist activity, despite adequate timing intake (Student’s t test: p=0.52). The mean between agonist and antagonist muscles, was onset latency of the antagonist activity was 51 described initially in patients with idiopathic (SD 12) ms before and was 46 (SD 15) ms with cerebellar degeneration involving vermal and alcohol (Student’s t test: p=0.64). The mean paravermal parts of the cerebellum.8 To our ratio of the rate of rise of agonist activity (AGO knowledge, the reduced rate of rise of antago- Q30) divided by the rate of rise of antagonist nist activity has not been shown in extracerebel- activity (ANTA Q30) was 0.97 (SD 0.09) in lar disorders. The defect in the tuning of the the basal state and was 0.97 (SD 0.09) with shape of the antagonist activity8 in the present alcohol (Student’s t test: p=0.70). The figure case indicated that the spinocerebellum was (A) illustrates the flexion movements of the probably the main site of the deleterious action right wrist in our patient before and after alco- of alcohol and its metabolites9 on cellular and hol intake. Mean movement amplitude was synaptic activity. Alternatively, alcohol could 14.5° and mean peak velocity was 570°/s in the have impaired activity of aVerent spinocerebel- basal state. With alcohol, movements were lar tracts or eVerent projections from the clearly hypermetric: the mean movement spinocerebellum. Moreover, inspection of indi- amplitude was 24.3°, and mean peak velocity vidual traces of antagonist EMG activities in was 579°/s.
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