Neurological Abnormality
Neurological Abnormality, Tardive Dyskinesia
and Parkinsonism
Background
Over the course of many decades, patients
with schizophrenia have consistently been observed to evidence an
increased frequency of neurological abnormality in the form of deviations
in motor coordination, sensory integration, and cognitive performance,
as well as deviations in reflexes and muscle tone. Examples of neuromotor
deviation are clumsiness in walking and poor balance, involuntary
movements such as twitching or shaking, and so-called ‘mirror
movements’ in one hand while performing a task with the other
hand. Increased rates of neurological abnormality are highly discriminatory
of schizophrenia patients. In one of our studies, a level of neurological
abnormality (> 6 points) that was found in only 1% of the normal
comparison subjects characterized 80% of the schizophrenia patients.
While these signs indicate a varying degree
of malfunction in the nervous system associated with schizophrenia,
the origin and meaning of these signs remain unclear. This neurological
abnormality may potentially result from genetic factors associated
with schizophrenia, early physical trauma in the form of obstetric
(pregnancy and delivery) complications or brain malformations, the
progression of the schizophrenia disease process itself, and/or
the treatment of the disease. Neuroleptic medications have typically
been considered to be the basis for involuntary movements termed
‘Tardive Dyskinesia’. Some schizophrenia samples also
show increased rates of signs of Parkinsonism, a phenomenon that
is typically related to medications or aging.
Nevertheless, extensive evidence suggests
that such neurological abnormality in schizophrenia patients frequently
already exists in childhood before the development of their schizophrenia,
and is also found with increased frequency in the mentally healthy
untreated close relatives of schizophrenia patients, even in childhood.
Some abnormal movements that are typically thought to be the result
of neuroleptic treatment (when seen in patients) are also observed
in patients’ relatives in childhood, i.e. in young individuals
who have neither been ill nor received any treatment. We have also
found a positive correlation between the amount of neurological
abnormality in the patient with schizophrenia and in the healthy
relatives in the same family, suggesting the influence of one or
more ‘familial factors’. While genetic factors might thus
appear to have primary importance, the neurological abnormality
in these relatives has in some samples been found to be associated
with a history of obstetric complications. We have also recently
found that signs of tardive dyskinesia are strongly related to a
history of obstetric complications (instead of neuroleptic medications
or a family history of psychosis) in relatively young patients with
schizophrenia.
Investigation in HUBIN
The purpose of investigating these areas
in HUBIN is to determine the extent and nature of the subjects’
neurological abnormality (including both so-called ‘hard’
and ‘soft’ neurological signs, and in four functional
neurological domains: neuromotoric, sensory, cognitive and primitive
reflexes), as well as possible signs of Tardive Dyskinesia and Parkinsonism.
This investigation permits a characterization of the level of practical/clinical
neurological disturbance in each individual, and the further study
of the possible genetic, early environmental and later environmental
influences on this disturbance.
The methods chosen for use in HUBIN are well-established
and have produced valuable and interesting findings in previous
research. The neurological assessment consists of 44 standardized
items (Ismail et al 1998a). This assessment is described in detail
in English and Swedish manuals, now in updated and revised form
(McNeil 2000). Detailed scoring sheets are available in both languages.
The total assessment (including Minor
Physical Anomalies) takes less than 1 h. Very satisfactory
inter-scorer agreement has been obtained for neurological assessment
(intraclass correlation coefficient = +0.87 to +0.97), tardive dyskinesia
(+0.96) and Parkinsonism (+0.96).
Relevant References:
Neurological Abnormality:
Ismail
B, Cantor-Graae E, McNeil TF. Neurological abnormalities in schizophrenic
patients and their siblings. American Journal of Psychiatry 1998;155:84-89.
Ismail
B, Cantor-Graae E, McNeil TF. Neurological abnormalities in schizophrenia:
clinical, etiological and demographic correlates. Schizophrenia
Research 1998;30:229-238.
Cantor-Graae
E, Ismail B, McNeil TF. Are neurological abnormalities in schizophrenic
patients and their siblings the result of perinatal trauma? Acta
Psychiatrica Scandinavica 2000;101:142-147.
Tardive Dyskinesia and Parkinsonism:
Simpson
GM, Lee JH, Zoubok B, Gardos G. A rating scale for tardive dyskinesia.
Psychopharmacology 1979;64:171-179.
Simpson
GM and Angus JWS. A rating scale for extrapyramidal side-effects.
Acta Psychiatrica Scandinavica 1970;212(suppl. 44):11-19.
Ismail
B, Cantor-Graae E, McNeil TF. Neurodevelopmental origins of tardive-like
dyskinesia in schizophrenia patients and their siblings. Schizophrenia
Bulletin 2001;27:629-41.
Project leader: Tom
McNeil
Co-workers: Monica
Hellberg, Lilian
Frygnell, Pontus Strålin
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