Absolutely. Cerebellar ataxia has been more than just ?associated?
with exposure to these chemicals, these compounds have been listed as
some of the many causative factors of cerebellar ataxia.
Before we go into the specifics of the association between toluene,
Trichloroethylene and other paint chemicals, let?s discuss the basics
of the condition, cerebellar ataxia:
The term cerebellar ataxia is an umbrella term for a group of
disorders affecting one region of the brain, the cerebellum. The
cerebellum?the namesake of the condition--is located at the base of
the brain and controls balance and coordination. Thus, disorders
affecting this region of the brain, such as cerebellar ataxia, present
with symptoms of lack of coordination and balance, but can entail
related signs, as well. These can include difficulty walking,
maintaining posture, the development of a type of tremor called
?action tremor? which presents when the individual attempts to reach
for a specific target, difficulties with speech or even swallowing,
incontinence and loss of sight.
Brain conditions like cerebellar ataxia are much more likely to have
gradual, rather than acute, onsets. This means that the symptoms
described above can come on so slowly and gradually, the sufferer may
not notice its existence until it becomes noticeable. Also in keeping
with the nature of brain disorders, cerebellar ataxia is progressive,
meaning the condition continues to advance rather than presenting and
remaining consistent or remitting.
While most cases of cerebellar ataxia are gradual in onset, there are
some types of the disorder which can come on with rapidity. The means
by which cerebellar ataxia presents itself can offer much to the
individual attempting to locate the cause.
Acute-onset cerebellar ataxia is actually most common in children,
following a viral infection such as chicken pox, Epstein-Barr or
Since your question involves exposure to chemicals in the 1980s, I
will focus more on the second type of cerebellar ataxia.
Chronic, progressive cerebellar ataxia also has a variety of causes
(or etiologies), all of which cause the presence of a lesion at the
site of the cerebellum. Lesions can be space-occupying or not.
Examples of causes of space-occupying lesions include vascular
processes, multiple sclerosis, etc. Other means by which lesions can
be produced in the cerebellar area include infectious, hereditary,
metabolic or due to exposure.
Since you directly question the possible correlation between chemical
exposure and cerebellar ataxia, this will be the focus of this answer.
Should you suspect, after reading this answer, your case to be of one
of the other above causes, we can discuss those, as well. Just let me
know. I am here to help. I, too, have suffered from a neurological
condition for years and know the pain and the fear that comes from the
cause being idiopathic, or unknown.
First, let?s look into cerebellar ataxia as it is associate with
exposure to toluene. This is such a known cause of cerebellar ataxia,
the associated condition is actually referred to as toluene-induced
neurological syndrome. A search on the National Institute of Health?s
site, Medline produces an almost innumerable amount of case studies
linking the two. Here are some excerpts and links:
?A 31-year-old woman presented slowly progressing ataxia and
neurasthenic symptoms after 14-year occupational exposure to low
concentration toluene vapour. Examination disclosed only cerebellar
signs. Cognitive functions were normal except moderate visuo-spatial
and constructive deficit. CT imaging showed severe pancerebellar
atrophy without pathological signs in other brain structures. Two
years after she was removed from workplace, CT imaging and ataxia
showed no worsening, while visuo-constructive function improved. The
authors warn against possible neurotoxic risk associated with this
kind of exposure.?
Here is a case study involving the effects of intentional, long-term
inhalation. I know your case is much different, but is, in effect, the
A twenty-nine-year old white man presented with complaints of
worsening coordination involving all four limbs, associated with
tremors off and on, for a period of eight months. The patient had a
history of toluene sniffing since the age of sixteen. He stopped five
months prior to presentation, with only slight improvement in his
ability to walk. He complained of continued unsteadiness and
staggering gait. There was no history of sensory deficits, pain or
memory loss. Neurologic examination revealed dysarthric speech with
intact cranial nerves, except for saccadic eye movement. Muscle
strength was 5/5 in all four limbs and the deep tendon reflexes were
well preserved. Sensory examination was completely normal. The
patient?s gait was ataxic and broad based with a positive finger-nose
test and an equivocal Romberg test. Significant tremors were present
at rest, which increased on intention. There was lack of co-ordination
of rapid alternating movements.
Fore more specific cases, you can follow the following Google search
link. I would keep listing them, but there are ? so many cases.
Let?s now move on to discuss the correlation between
trichloroethylene. Unfortunately, the findings are very similar:
?In a study of 50 workers employed from 1 month to 15 years in various
industrial cleaning and degreasing operations using TCE, complaints
due to chronic exposure included decreased appetite, sleep
disturbances, ataxia, vertigo, headache, short-term memory loss, and a
reduced number of word associations. Greater frequency of symptoms was
noted in workers exposed to higher (85 ppm) than lower (14 ppm) mean
Chronic occupational TCE exposure has been associated with neurologic
Some of the observed neurologic effects from long-term exposure to TCE
indicate impaired trigeminal nerve function (e.g., blink reflex and
masseter reflex). In the brains of animals chronically exposed to high
concentrations of TCE (1,000 to 3,000 ppm), histologic changes have
been demonstrated. Persons who have deliberately abused volatile
chlorocarbon solvents have developed cerebellar damage and ataxia.?
The way the last paragraph has been worried is bothersome, because it
seems to attempt to present the results of ataxia as being only from
intentional inhalation and exposure, though the first paragraph
clearly states that there is an obvious risk of developing cerebellar
ataxia through workplace exposure.
?A clinical picture of cerebellar syndrome with cerebellar atrophy
revealed by CT scan in a worker for 28 years occupationally exposed to
petrol and trichloroethylene vapours has been described. The
relationship between the illness and the occupational exposure to the
organic solvents has been discussed.?
Here is WONDERFULLY thorough study of the solvent and how it can affect your body:
I don?t want to bombard you with too much more. In sum, the
relationship between these two chemicals and cerebellar ataxia is
quite apparent, and if you had been exposed to these chemicals in your
work place, there is a good chance that you could file suit to recover
damages incurred from this exposure.
Good luck to you and your endeavors. I am here for you, if you have
more you would like to know.
?cerebellar ataxia? + symptoms
?cerebellar ataxia? onset
?cerebellar ataxia? acute
?cerebellar ataxia? gradual
?cerebellar ataxia? + toluene + exposure
?cerebellar ataxia? + Trichloroethylene + exposure