Craniofacial Muscles

296 J. Park et al.
Focal motor seizures can include paroxysmal eyelid movements, such as
fl uttering, which occurs during the seizure. Unilateral facial movements or eyelid
closure which is repetitive, brief, and followed by weakness (Todd’s paralysis)
would suggest a focal motor seizure involving the face. Spread to the hands or
limbs, or generalization to involve the other side of the face or body with loss of
consciousness, would make this diagnosis obvious. Evaluation consists of an electroencephalogram
(EEG) and neuroimaging to detect a structural seizure focus,
followed by treatment with anticonvulsants.
16.6 Psychological Problems
Depression, anxiety, and personality disorder are often associated with
blepharospasm, but it is generally regarded that blepharospasm can cause or aggravate
the psychological problems. The variability in severity of symptoms, the
unusual aggravating and relieving factors, and the discrepancy between the history
of the disorder and objective signs seen by the physician have often resulted in the
condition being misdiagnosed as hysteria or other psychiatric disorders.
Blepharospasm used to be considered a psychological disorder but is now thought
only rarely to be due to psychogenic factors. However, sudden onset spasms in
young patients under 30 may represent psychological blepharospasm.
16.7 Drug-Induced Facial Dyskinesias (Tardive Dyskinesia)
The classic form of tardive dyskinesia, caused by long-term treatment with neuroleptics
(anti-dopaminergics), involves the buccal–lingual–masticatory area, most
frequently and usually spares the eyelids; tardive dyskinesia may consist of rapid,
continuous, stereotyped, writhing movements of the orofacial region, and may
involve either bilateral or unilateral blepharospasm.
Commonly used drugs that are implicated in tardive dyskinesia include antidopaminergics
or neuroleptics (e.g., haloperidol), dopaminergics or anti-Parkinson’s
agents (e.g., levodopa), antidepressant and anxiolytics (e.g., alprazolam), antiepileptics
(e.g., carbamazepine, phenytoin), antiemetics (e.g., metoclopramide), nasal
decongestants containing histamine, and anticholinergics (Levin and Reddy 2000 ) .
The reported duration of exposure that incites tardive dyskinesia ranges from 3 days
to 11 years, with an average of about 3.7 years, and onset of the dyskinesia can
occur up to 1 year after cessation of the offending drug (Jankovic 1985 ) .
The movements associated with this disorder differ from those of cranial dystonia
in that the movements are choreic rather than sustained or dystonic and are often
quite stereotypic (Tarsy 2000 ) . However, neuroleptics can also cause a chronic form
of dyskinesia that mimics cranial dystonia (tardive cranial dystonia) which is dif fi cult
to differentiate from essential blepharospasm. It is most important to check to see if