Alcohol & Alcoholism Vol. 33, No. 4, pp. 393-402, 1998
ATAXIA OF STANCE IN DIFFERENT TYPES OF ALCOHOL
DEPENDENCE — A POSTUROGRAPHIC STUDY
CHRISTIAN WOBER*, CICEK WOBER-BINGOL, ANDREAS KARWAUTZ 1 ,
AMANDA NIMMERRICHTER1, HENRIETTE WALTER 2 and LUDER DEECKE
Department of Neurology, University of Vienna, 'Anton Proksch Institute. Vienna and 2Department of Psychiatry, University
of Vienna, Austria
(Received 10 November 1997; in revised form 6 February 1998; accepted 23 February 1998)
Abstract — The aim of this study was to assess the prevalence of ataxia of stance in different types of
alcohol-dependent patients. Posturographic measurements were performed in 82 abstinent alcoholdependent patients and 54 healthy controls in order to analyse postural control According to Lesch and
co-workers, alcohol dependence was classified as total abstinence (Type I), drinking without loss of
control (Type II), fluctuating course (Type III), and persistent severe drinking (Type IV). The
mechanisms of alcohol dependence in these subtypes can be summarized as follows: Type I patients
drink alcohol to counteract symptoms of alcohol withdrawal; Type II patients use alcohol as an agent for
solving conflicts; Type III patients drink alcohol to 'treat' an affective disorder, and Type IV patients
have a history of pre-alcoholic neurological and/or psychiatric disorders. The neurological examination
showed pathological findings in 39%, whereas posturographic measurements uncovered impaired
postural control in 61% (y_~ = 8.8, P = 0.003). Comparing the different study groups revealed that ataxia
of stance was most common in alcohol-dependent patients classified as Type IV (T = 0.24, P = 0.005).
In conclusion, posturographic measurements are superior to the clinical examination in detecting
postural imbalance in alcohol-dependent patients. The prevalence of postural imbalance is highest in
patients classified by Lesch as Type IV. Consequently, this type of alcohol dependence — characterized
by pre-alcoholic neurological and/or psychiatric disorders, bears the highest risk of developing ataxia of
INTRODUCTION
Among alcohol-related neurological disorders,
impaired postural control occurs not only as die
immediate dose-dependent effect of alcohol intake
(Schuckit, 1985; Lex et al., 1988; Kubo et al,
1990; Ledin and Odkvist, 1991a; Monteiro et al,
1991; Bauer and Hesselbrock, 1993; Goebel et al.,
1995; Schuckit et al., 1996), but also as a consequence of chronic alcohol intoxication (Diener
et al., 1984; Scholz et al, 1986; Ledin and
Odkvist, 1991i>). The control of upright posture
requires: (1) neuronal pathways which process
visual, vestibular and proprioceptive inputs; (2)
complex motor programmes involving cerebellar,
pyramidal, and extrapyramidal functions; (3) an
adequate neuromuscular response. Impairment of
postural control in alcohol dependence may be
*Author to whom correspondence should be addressed at:
Universitatsklinik ftlr Neurologic Wahringer GUrtel 18-20,
A-1090 Wien, Austria.
caused by cerebellar dysfunction and/or peripheral
neuropathy. The cerebellar dysfunction is morphologically related to an atrophy of the anterior
lobe of the cerebellum. Clinically, it is associated
with a predominant ataxia of stance and gait, and
posturographically, it is characterized by an increased antero-posterior body sway with a frequency of 3/s which can be compensated partially
by visual control (Diener et al., 1984; Scholz et al.
1986). Alcoholic peripheral neuropathy is due to
axonal nerve damage, and it is associated with
increased vibratory perception thresholds, abolished ankJe jerks, and hypaesthesia (Behse and
Buchthal, 1977). Until now, however, there is a
lack of information about factors predicting the
risk of postural imbalance in alcohol-dependent
patients and none of the earlier posturographic
studies distinguished between different types of
alcohol dependence. Such differentiation, however, is essential since alcohol dependence does
not represent a homogeneous disorder, but a complex development producing various clinical
393
© 1998 Medical Council on Alcoholism
394
C. WOBER et al.
pictures with differing symptom constellations
requiring different therapeutic approaches.
Multivariate aetiologic models have described
alcohol dependence as a developmental interaction between toxic effects of alcohol, personality
traits, and social surroundings (Glatt, 1982;
Vaillant, 1983; Lesch, 1985). Accordingly, efforts
have been made to define subtypes of alcohol
dependence in order to estimate the prognosis of
each individual patient and to define specific
treatment goals. Bowman and Jellinek (1941)
distinguished four groups of alcoholics based on
drinking behaviour. More recently, Cloninger et
al. (1981) identified two types of alcohol dependence: Type I alcoholics were characterized by a
late onset of alcohol dependence, provoked by
environmental factors in persons with high harm
avoidance, low novelty seeking, and high reward
dependence, whereas Type II alcoholics were
observed to exhibit alcohol-seeking behaviour
early in life, based on strong heritable influences
independent of the environment and showing an
impulsive, risk taking, antisocial behaviour.
Morey and Skinner (1986) differentiated three
types of alcoholics designated as early stage
problem drinkers, affiliative drinkers, and schizoid
drinkers. Zucker (1987) described four types of
alcohol dependence and distinguished between (1)
antisocial, (2) developmental^ cumulative, (3)
negative affect, and (4) developmental^ limited
alcoholism. Babor (1992) developed a system of
Type A and Type B alcoholism: Type A was
characterized by late onset, fewer childhood risks,
less severe dependence, fewer alcohol-related
physical and social consequences, less previous
treatment for alcohol problems, less psychopathological dysfunction, and less distress in the areas
of work and family. Type B, on the other hand,
was characterized by earlier onset, more childhood
and familial risk factors, greater severity of dependence, polydrug use, more serious consequences, a
chronic treatment history and more life stress and
psychopathological dysfunction.
Lesch (1985), Lesch et al. (1988), and Lesch
and Walter (1996) have developed a classification
system, or typology (Types I to IV) based on a
prospective study in 444 patients, which considered a series of features including parental factors,
physical, psychological and social development of
the patient, drinking behaviour, biochemical
characteristics, psychiatric factors, and neurologi-
cal disorders. According to Lesch's classification,
Type I patients drink alcohol to counteract
symptoms of alcohol withdrawal. Type II patients
use alcohol as an agent for solving conflicts and
reducing anxiety. Type in patients drink alcohol
to 'treat' an affective disorder and may consider
alcohol as an antidepressant. Both Type II and
Type III patients experience mild to moderate
withdrawal symptoms in the late stages of alcohol
dependence. Type IV patients have a history of
cerebral damage that precedes the development of
alcohol dependence and alcohol withdrawal
causes severe psychopathological symptoms in
these patients. Considering the prognosis, it is
possible to define reliable treatment strategies
specifically for each type of alcohol dependence
(Lesch and Walter, 1996; Lesch et al., 1996,
1997). Type I can be classified as an abstinent
course, Type n as drinking without loss of control,
Type III as a fluctuating course, and Type IV as
persistent severe drinking. Accordingly, one can
hypothesize that the neurological outcome is
poorest in Type IV patients. In the present study,
we wanted to test this hypothesis focusing on
postural control. We were interested in clarifying
whether postural imbalance increases from healthy
subjects to Type IV alcohol dependence and
whether pre-alcoholism neuropsychiatric disorders, which represent the underlying pathogenic
mechanism in Type IV patients, are a predisposing
factor of ataxia of stance in alcohol-dependent
patients.
PATIENTS AND METHODS
We included 82 patients fulfilling the diagnostic
criteria of alcohol dependence according to DSMIV (American Psychiatric Association, 1994) and
ICD-10 (World Health Organization, 1992). The
severity of alcohol dependence was quantified by:
(1) the duration of the disease; (2) alcohol consumption during the 6 months before admission
for withdrawal therapy; (3) estimated lifetime
alcohol consumption. The latter was calculated by
following the formula published by Estrin (1987),
as follows:
Lifetime alcohol consumption = [kg of daily
ethanol consumption] x [days/month drinking] x [(months since onset of alcohol dependence) - (months of abstinence)]
POSTUROGRAPHY IN ALCOHOL DEPENDENCE
395
All patients underwent in-patient withdrawal
therapy at the same institution (Anton Proksch
Institute, Vienna, Austria) and had finished
organic withdrawal at least 2 weeks prior to this
investigation. To classify the type of alcohol
dependence cross-sectionally, we used a semistructured interview, a psychiatric exploration, and
a neurological examination (Lesch, 1985; Lesch et
al, 1990; Plinius Major Society, 1994). Each
patient was assigned to the appropriate type of
alcohol dependence following a decision tree
published elsewhere (Lesch et al., 1990, 1996).
The neurological features in this decision tree
included alcohol-related disorders, such as withdrawal symptoms, seizures, peripheral neuropathy,
and cognitive impairment, as well as disorders not
related to alcohol, e.g. a history of perinatal
cerebral damage, febrile convulsions, head injury,
meningitis, or encephalitis. The psychiatric features covered psychological withdrawal symptoms, affective disorders, depressive symptoms,
sleep disorders, suicidal thoughts, personality
traits such as aggressive behaviour, oligophrenia
and several others. Assigning an individual patient
to the appropriate type of alcohol dependence
starts with checking whether he/she fulfils the
criteria of Type IV followed by Types HI, I, and n.
The characteristics of the drinking behaviour, the
social, psychological, and somatic features as well
as the supposed main pathogenic factor in each of
the four types of alcohol dependence were
summarized elsewhere (Lesch et al., 1988, 1996).
impaired postural control by any strategy, except
external support, provided that the position of the
feet remained unchanged. One measurement
period lasted 20 s. We performed 20 measurements per patient, 10 with eyes open and 10 with
eyes closed. In the 'eyes open' condition, the
patients viewed a black disc (diameter 10 cm)
fixed to the wall 2 m in front of their eyes.
The posturographic equipment consisted of a
force measuring platform with piezo-electric strain
gauges in all four corners connected to an
electronic control unit (Toennies Medical Electronics, Freiburg, Germany) and a personal
computer. The strain gauges registered the micromotions of body sway projected to the centre of
foot pressure (CFP). Before the first measurement,
a normalizing procedure was completed to compensate for body weight. The signals visualized
represented the distance the CFP vector was
travelling during 1 s and the area covered by the
movement of the vector. The result of the
measurement was a sway direction diagram
characterized by four sway parameters: sway
path, sway area, antero-posterior sway, and lateral
sway. To obtain the direction of body sway, it was
necessary to divide the circle of possible sway
directions into eight segments. The vectors resulting from the displacement of the CFP from the
centre of the platform were summed up within the
eight segments, according to their directions.
Thus, body sway could be visualized, quantified,
and analysed sensitively, simply, and accurately.
To quantify and analyse body sway, measurements on a posturographic platform (Kollegger et
al., 1992; Wober et al., 1993) were performed.
Patients with uncorrectable severe reduction of
visual acuity, double vision, peripheral vestibular
lesions, pareses of the lower limbs not related to
alcoholic peripheral neuropathy, sequelae of bone
features interfering with postural equilibrium, and
patients who did not cooperate sufficiently during
the examination were excluded. In addition,
patients who had experienced delirium tremens
within 2 months of the examination were also
excluded.
Posturography was carried out in a quiet, welllit, comfortably heated room. The subjects were
barefoot and were told to stand on the posturographic platform in an upright position in as stable
manner as possible, arms at the side, feet 4 cm
apart. They were allowed to compensate for
The control group consisted of 54 healthy
subjects similar in age and gender. All control
subjects showed normal neurological findings.
They consumed less than 40 g of alcohol/day
and none had a history of alcohol abuse or
dependence. The protocol of the posturographic
measurements was the same as in the patient
group and normal values were defined as the
mean + 2 SD.
For calculations and statistical analysis, SAS
software (SAS Institute Inc, 1985) was used. To
analyse the demographic and clinical data, Kendall
T correlation coefficients and •/} tests were applied
as appropriate. In each of the eight posturographic
parameters, i.e. sway path, sway area, anteroposterior and lateral sway during stance with eyes
open and eyes closed, the mean of the 10
measurements in each patient was used for further
calculations. To examine the hypotheses that
396
C. WOBER et al.
Table 1. Demographic findings, duration of alcohol dependence, alcohol intake during the 6 months before admission for
withdrawal therapy and estimated lifetime alcohol consumption in four types of alcohol dependence
Statistics
Alcoholism type
Type I
("=17)
Type II
(" = 21)
Type HI
(n = 26)
TypeFV
(n =18)
39.8 ± 8.5
16/1
9.3 ± 1.2
41.0 ± 9.2
17/4
9.3 ± 1.2
41.6 ± 10.0
24/3
9.1 ±0.8
41.1 ± 9.7
17/0
9.3 ± 1.0
11
6
0
0
14.8 ± 10.2
11
5
2
3
10.5 ±6.1
14
7
1
4
12.4 ± 6.8
6
6
4
2
17.7 ±9.8
64.8 ± 19.3
55.4 ± 22.2
59.2 ±22.1
70.2 ± 19.8
1684 ± 1271
1095 ± 783
1377 ± 868
2395 ±1271
Demography
Age (mean ± SD)
Sex (male/female)
Education (years, mean ± SD)
Profession
Skilled
Unskilled
Unemployed
Retired
Duration of alcohol dependence
(years, mean ± SD)
Pre-admission alcohol consumption (kg, mean ± SD)
Lifetime alcohol consumption
(kg, mean ± SD)
T = 0.02
/ 2 = 4.40
T = 0.02
n.s.
n.s.
n.s.
/ 2 = 5.61
T = 0.12
n.s.
n.s.
T = 0.04
n.s.
T
= 0.22
P -= 0.009
For statistical analysis, Kendall T correlation coefficients and •/_ tests were calculated, n.s. Denotes not significant.
postural imbalance is related to the type of alcohol
dependence and that this imbalance increases from
healthy subjects to patients classified as Type IV,
Kendall T correlation coefficients were calculated.
Kendall T correlation coefficients were also
calculated to analyse the relations between alcohol
consumption, clinical, and posturographic findings. For these calculations, the pathological
posturographic values were summed. Accordingly,
each patient had a score between zero (all
posturographic parameters < mean + 2 SD) and
eight (all parameters > mean + 2 SD). The level of
statistical significance was fixed at P < 0.05.
RESULTS
Classification of alcohol dependence
According to the criteria of Lesch (1985), Lesch
et al. (1988), and Lesch and Walter (1996), 17
patients were classified as Type I, 21 as Type II,
26 as Type m, and 18 patients as Type IV. The
durations of alcohol dependence and daily alcohol
consumption prior to admission for alcohol withdrawal therapy were similar in all four types. The
estimated lifetime alcohol consumption, however,
was highest in Type IV and much lower in the
other types and this finding was statistically
significant (Table 1).
Demographic findings
The mean age of the patients was 41 ±9.3 years
(range 20-67 years), which did not differ between
the four subtypes. Only a small minority of
patients (8 out of 82) were females. The level of
education was similar in all subtypes, only eight
patients had completed more than 9 years of
school. The majority of patients were skilled
(n — 42) or unskilled workers (n = 24). Unemployment or retirement (because of alcohol
dependence) was found most frequently among
patients classified as Type IV and least frequently
among those classified as Type I, but this
difference was not statistically significant (Table
1)Neurological findings
The clinical neurological examination revealed
normal findings in 52 patients (63.4%), symptoms
and/or signs of alcoholic neuropathy in 29 (35.4%)
and cerebellar signs in nine patients (11%). Eight
of these patients had both neuropathic and
cerebellar signs. The prevalence of neuropathy
showed a statistically significant increase from
Type I to Type IV. The prevalence of cerebellar
signs and other neurological abnormalities was
also highest in Type IV, but these differences did
not reach the level of statistical significance.
POSTUROGRAPHY IN ALCOHOL DEPENDENCE
Table 2. Sway path (cm/s) during upright stance with eyes
open and closed in healthy controls and four types of
alcohol-dependent patients
397
Table 4. Antero-posterior sway (cm/s) during upright stance
with eyes open and closed in healthy controls and four
types of alcohol-dependent patients
Alcoholism type
Condition and
parameters
Eyes open
Maximum
Upper quartile
Median
Lower quartile
Minimum
Eyes closed
Maximum
Upper quartile
Median
Lower quartile
Minimum
Type
Controls
I
Type
II
Type
III
Alcoholism type
Type
rv
1.59
1.38
1.16
0.93
0.55
1.64
1.43
1.09
1.01
0.72
4.92
1.90
1.26
0.94
0.75
5.71
1.79
1.16
0.91
0.79
5.66
3.08
1.67
1.41
0.99
3.22
1.97
1.49
1.18
0.61
3.84
1.95
1.70
1.28
1.01
14.10
260
1.65
1.16
0.80
12.12
2.66
1.71
1.30
0.86
16.24
7.81
2.88
1.84
1.22
Table 3. Sway area (cm /s) during upright stance with eyes
open and closed in healthy controls and four types of
alcohol-dependent patients
Condition and
parameters
Eyes open
Maximum
Upper quartile
Median
Lower quartile
Minimum
Eyes closed
Maximum
Upper quartile
Median
Lower quartile
Minimum
Type
Controls
I
Eyes open
Maximum
Upper quartile
Median
Lower quartile
Minimum
Eyes closed
Maximum
Upper quartile
Median
Lower quartile
Minimum
Type
Type
m
rv
0.25
0.15
0.12
0.10
0.07
0.30
0.23
0.19
0.15
0.09
1.43
0.39
0.19
0.16
0.10
1.52
0.33
0.19
0.13
0.11
1.47
0.63
0.28
0.24
0.19
0.58
0.25
0.18
0.12
0.09
0.92
0.38
0.30
0.22
0.13
5.36
0.54
0.30
0.25
0.10
3.27
0.50
0.30
0.19
0.11
3.68
1.16
0.59
0.32
0.25
Table 5. Lateral sway (cm/s) during upright stance with
eyes open and closed in healthy controls and four types of
alcohol-dependent patients
Alcoholism type
Condition and
parameters
Type
II
Alcoholism type
Controls
Type
I
Type
II
Type
III
Type
IV
0.38
0.25
0.17
0 12
0.04
0.29
0.21
0.19
0.12
0.07
0.97
0.39
0.19
0.13
0.08
1.41
0.34
0.21
0.13
0.08
1.16
0.48
0.31
0.22
0.13
1.07
0.40
0.25
0.16
0.04
0.86
0.36
0.25
0.16
0.11
3.91
0.53
0.24
0.17
0.07
4.47
0.47
0.28
0.19
0.10
8.37
2.21
0.53
0.32
0.16
Posturographic findings
In 32 patients (39%), all posturographic parameters were within the normal range, whereas in
50 patients (61%), at least one parameter was
increased pathologically. With eyes open, sway
path (Table 2) was increased in 25 patients
(30.5%), sway area (Table 3) in 17 (20.7%),
antero-posterior sway (Table 4) in 43 (52.4%), and
lateral sway (Table 5) in three patients (3.7%).
With eyes closed, sway path was increased in 28
patients (34.1%), sway area in 21 (25.6%), anteroposterior sway in 44 (53.7%), and lateral sway in
Condition and
parameters
Eyes open
Maximum
Upper quartile
Median
Lower quartile
Minimum
Eyes closed
Maximum
Upper quartile
Median
Lower quartile
Minimum
Controls
Type
I
Type
11
Type
III
Type
IV
0.26
0.20
0.17
0.11
0.07
0.20
0.16
0.10
0.09
0.07
0.19
0.15
0.12
0.09
0.06
0.31
0.18
0.12
0.10
0.06
0.33
0.22
0.17
0.11
0.07
0.33
0.28
0.21
0.11
0.06
0.28
0.19
0.14
0.09
0.06
5.32
0.16
0.14
0.10
0.05
3.59
0.22
0.16
0.10
0.14
3.97
0.43
0.24
0.13
0.07
six patients (7.3%) (Tables 2-5). The percentage
of pathologically increased posturographic values
increased from 13.2% in Type I to 54.2% in Type
IV and the percentage of patients with more than
one pathological posturographic parameter increased from 35.3% in Type I to 100% in Type
IV (T = 0.32, P = 0.0003). Sway path, sway area,
and antero-posterior sway increased significantly
from healthy subjects to patients classified as Type
IV, whereas lateral sway was similar in the five
study groups (Tables 2-5, Figs 1-4). In addition,
postural imbalance was consistently more pro-
398
C. WOBER el al.
Sway path
I
o
U
Eyes open
Eyes closed
Fig. 1. Median, upper, and lower quartile of sway path during upright stance with eyes open and eyes closed in healthy
controls and four types of alcohol dependence.
***/>< 0.001.
Sway area
2,5 -i
2***
*•
i«-
••••
.
*
Type III
• • - ? • • •
Typell
Type IV
Type III
Typell
Typel
Eyes open
•
Typel
r
0-'
Controls
. • • * • • •
.
frr
Controls
. - • •
:.i::...l
Type IV
0,5-
Eyes closed
Fig. 2. Median, upper, and lower quartile of sway area during upright stance with eyes open and eyes closed in healthy
controls and four types of alcohol dependence.
**P < 0.01; •**/> < 0.001.
nounced during stance with eyes closed than with
eyes open (Figs 1-4).
Relation of clinical and posturographic findings
Impaired postural control was uncovered by
posturographic measurements significantly more
often than by purely clinical assessment {•/} = 8.8,
P = 0.003). Pathological posturographic findings
were found in 46.2% of patients with normal
neurological findings, in 82.8% of patients with
signs of alcoholic neuropathy, and in 88.9% of
subjects with cerebellar signs. Postural imbalance
was strongly related to the presence of peripheral
neuropathy (T = 0.38, P = 0.0001) as well as to
the presence of cerebellar signs (T = 0.30,
P = 0.001).
Relation of clinical findings and alcohol
consumption
The alcohol consumption during the 6 months
before admission for withdrawal therapy was
related neither to the prevalence of peripheral
POSTUROGRAPHY IN ALCOHOL DEPENDENCE
399
Antero-posterior sway
1,2 0,9 -
"I 0,6 -
.-*
0,3 0
X
H
o
|
O
t-
o
U
H
H
H
s
£
Eyes closed
Eye* open
Fig. 3. Median, upper, and lower quartile of antero-posterior sway dunng upright stance with eyes open and eyes closed in
healthy controls and four types of alcohol dependence.
***P < 0.001.
Lateral sway
1,2 -i
0,9-
| 0,6 0,3 -
^^^4^0
S
£S
>•
i I I I i
Eyes open
rrrr-^
15 SfO
"^
H
H
Eyes closed
Fig 4. Median, upper, and lower quartile of lateral sway during upright stance with eyes open and eyes closed in healthy
controls and four types of alcohol dependence.
neuropathy (T = -0.06, P = 0.5) nor to the prevalence of cerebellar signs (T = 0.03, P = 0.7). By
contrast, the estimated lifetime alcohol consumption was related to peripheral neuropathy
(T = 0.24; P = 0.007), but not to cerebellar signs
(T = 0.10; P = 0.3).
the number of pathological posturographic values
(T = 0.07; P = 0.4). Increased lifetime alcohol
consumption, however, was associated with inCTeased postural imbalance (T = 0.26; P = 0.001).
Relation of posturographic findings and alcohol
consumption
Similar to the clinical findings, the pre-admission alcohol consumption level was not related to
This study on postural control in abstinent
alcohol-dependent patients, showed pathological
posturographic findings in more than 60% of all
patients and in almost 50% of those with normal
DISCUSSION
400
C. WOBER el al.
clinical neurological findings. Impaired postural
control was associated with the type of alcohol
dependence and occurred most frequently in
Lesch's Type IV (Lesch, 1985; Lesch et al,
1988; Lesch and Walter, 1996), and less often in
Types I, II, and III, even though the alcohol
consumption prior to admission for alcohol withdrawal therapy was similar in ail four types. This
discrepancy may be explained by differences in
the underlying pathogenic mechanisms. Type I
patients are characterized by a primary organic
weakness, Type II by a developmental disturbance, and Type III by sociopathic development.
Type IV patients have a history of neurological
and psychiatric disorders (which precede the
development of alcohol dependence) as well as a
developmental disturbance. However, Type IV
patients also had the highest lifetime alcohol
consumption. Accordingly, impaired postural control in Type IV may be the consequence of both
pre-alcoholic neurological damage and a certain
type of alcohol dependence.
Concerning the importance of demographic
data, the small number of women included did
not allow us to examine gender differences. Age
and onset of alcohol dependence were similar in
all four types. This finding is in contrast to other
typologies (Cloninger et al, 1981; Babor et al,
1992), which use these parameters as diagnostic
features.
The pattern of postural imbalance was similar to
that reported by Diener et al. (1984) and Scholz et
al. (1986). The percentage of pathological posturographic findings was also comparable to
earlier reports (Scholz et al, 1986). However,
our study is the first to demonstrate that the
prevalence of postural imbalance is not evenly
distributed among patients fulfilling the criteria of
alcohol dependence, but that a well-defined group
characterized by pre-alcoholic neurological and/or
psychiatric disorders (Lesch's Type IV) is predominantly afflicted.
The prevalence of alcohol-related neuropathy
was also related to the type of alcohol dependence,
showing the highest prevalence in Type IV. The
overall percentage of patients with neuropathy was
within the range reported in the literature. In our
study, 29 out of 82 patients (35.4%) had signs of
peripheral neuropathy consisting of reduced vibration sense and absent ankle jerks in 75.9%, more
severe sensory deficits in 13.8% and pareses in
10.3%. Scholz et al. (1986) found clinical signs of
peripheral neuropathy in 45% and Tuck and
Jackson (1991) reported a prevalence of 34%.
Investigating the vibration sense in alcoholdependent patients and healthy controls, Sosenko
et al. (1991) found increased thresholds in 18% of
younger and 47% of older alcoholic subjects.
Palliyath and Schwartz (1993) reported findings
which suggest that peripheral nerve functions
improve in chronic alcoholic patients with abstinence. In agreement with this report, Monforte et
al (1995) have shown that peripheral neuropathy
in alcohol-dependent patients is due to a doserelated toxic effect of alcohol. Similarly, we found
an association between the lifetime consumption
of alcohol and peripheral neuropathy.
The lack of an association between cerebellar
signs and type of alcohol dependence might be
explained by the small number of patients, since
the raw data showed at least a trend towards an
increase of cerebellar signs from Type I to Type
IV. Concerning the pre-admission and lifetime
alcohol consumption, however, there was not even
a trend associated with the prevalence of cerebellar signs. Similarly, a comparison between ataxic
and non-ataxic alcohol-dependent patients (Estrin,
1987) revealed no relation between alcohol consumption and ataxia. On the contrary, the ataxic
patients showed even less alcohol consumption
than the non-ataxic controls, suggesting that
alcoholic cerebellar degeneration is not a dosedependent phenomenon. This hypothesis, however, seems to be contradicted by reports that
ataxia in alcoholic cerebellar atrophy may
improve through abstinence (Diener et al, 1984;
Leblhuber et al, 1985).
Examining the relation between clinical and
posturographic findings demonstrated clearly that
posturographic measurements are superior to the
clinical assessment in detecting postural imbalance. The issue of the causal relation between
peripheral neuropathy, cerebellar signs, and postural imbalance remains controversial, however.
Melgaard and Ahlgren (1986) suspected that
peripheral neuropathy contributes to the ataxia in
alcohol-dependent patients. Scholz et al (1986),
however, found no correlation between the
severity of peripheral neuropathy and the severity
of cerebellar dysfunction, and concluded that
cerebellar damage and peripheral neuropathy
result from different mechanisms of alcohol
POSTUROGRAPHY IN ALCOHOL DEPENDENCE
401
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Troop, Institute of Psychiatry, London, for correcting the
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