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A case that combines cerebral eyelid ptosis and blepharospasm secondary to cerebral hemisphere infarction is shown. EMG recording from the facial and eyelid muscles revealed lack of the levator palpebrae superioris, orbicularis oculi and corrugator muscles activity. Any voluntary opening attempt lead to a simultaneous contraction of the three muscles. Blink reflex responses were normal although showed facilitation features on the right side and mild inhibition characteristics from the left side. Median nerve SEP revealed a loss of precentral components (P22-N30) as well as a delay and amplitude decrease of N20. Transcranial magnetic stimulation disclosed a complete lesion of corticospinal pathway for right upper limb. In this case, a right hemisphere lesion caused an unusual eyelid motor abnormality: cerebral eyelid ptosis and blepharospasm induced by the voluntary eyelid opening.

Dyskinesias are one of most frequent motor complications of parkinsonian patients on chronic levodopa treatment. This article reviews their clinical characteristics, risk factors, pathophysiology and possible therapeutical approaches.

More effective measures to control and replace the dopaminergic deficit of Parkinson's disease are being actively sought. One basic problem is how the striatal dopamine loss should be replaced in order to mimic most accurately the physiological state. Animal electrophysiology indicates that the dopaminergic nigrostriatal pathway has a dual tonic and phasic action. Intermittent dopaminergic stimulation is associated with behavioural hyposensitivity both in animal models and in patients with Parkinson's disease. Continuous dopaminergic stimulation provides a tonic background and improves some clinical problems but is also associated with tolerance. None of the available pharmacological approaches can restore the dopamine deficiency of Parkinson's disease to physiological levels. Continuous dopaminergic stimulation for < 24 h, associated with small doses of levodopa or a short-acting dopamine agonist, appears to be the best, albeit imperfect, therapeutic approach until other, more efficacious remedies are developed.

We studied the histories of 173 patients with Parkinson's disease (1985-1987) chronically treated with levodopa + dopa decarboxylase inhibitor. Ninety four patients had daily motor fluctuations and 79 showed stable motor response. The most significant differences between fluctuating and stable patients were given by age at disease onset and duration of levodopa therapy. Patient with disease onset before 60 had a greater risk (p less than 0.001) of developing fluctuations. Delaying the initiation of levodopa treatment was not associated with a smaller incidence of fluctuations.

Blepharospasm is a cranial dystonia characterized by forceful spasms of the orbicularis oculi muscle which may lead to functional blindness in approximately two-thirds of patients. Botulinum toxin injection is a simple procedure, very effective and with little morbidity. It is considered as the treatment of choice for patients with disabling blepharospasm.

The response to different therapeutic methods was evaluated in a series of 264 patients with blepharospasm. The most effective drug therapy were anticholinergic agents, which resulted in the initial improvement of symptoms in 20% of treated patients. There was improvement in isolated cases treated with levodopa, dopaminergic agonists, neuroleptics, benzodiazepines and tricyclic antidepressants. Bilateral avulsion of the facial nerve was carried out in 29 patients; 27 of these (93%) improved. Spasms relapsed in 22 cases, after a mean period of 12 months. Myectomy of the orbicular muscle was performed in 8 patients. In only 2 cases some improvement was obtained. One hundred and fifty-one patients were treated with infiltrations of botulinum toxin A in the orbicular muscle. 78% of cases improved. The mean duration of the benefit of each injection was 9.2 weeks. The most common secondary effects were local (ptosis, diplopia) and transient.

Two hundred and seventy-two patients with idiopathic blepharospasm were reviewed to establish the role of local eye disease in their illness. The majority of patients (57%) had symptoms at the onset of their illness such as dryness of the eyes, grittiness, irritation or photophobia suggesting eye lid or ocular surface disease. Detailed ophthalmological examination at the time of presentation had been carried out in 170 of the 272 cases; 64% of these patients had ocular symptoms, and 40% had demonstrable ocular surface or eye lid pathology. Such pathology was usually bilateral, chronic and resistant to local treatment. Blepharospasm developed in these patients after a long latent period, often of many years. Unilateral pathology was acute, normally responded well to local treatment, but was followed by the development of bilateral blepharospasm usually within six months. Amongst all 272 patients, those without ocular symptoms at presentation rarely developed them subsequently; if they did, there were no abnormal signs. The data suggest that ophthalmological disorders may trigger idiopathic blepharospasm in a substantial proportion of cases predisposed to develop this condition.

Fluctuations and dyskinesias are the 2 main motor complications associated with chronic levodopa therapy. Striatal denervation following degeneration of the substantia nigra dopaminergic projections is probably the major pathophysiologic mechanism underlying motor fluctuations. In addition, pathologic modification of striatal receptors, partially related to the nonphysiologic delivery of levodopa in a discontinuous pulsatile mode, may be responsible for the various types of dyskinesias and sudden "off" episodes. Drugs capable of providing a stable dopaminergic stimulation should be particularly useful for preventing the development of motor complications in patients not yet treated. At the other end of the clinical spectrum, patients with complex fluctuations are the least likely to improve with slow-release levodopa preparations.

PHNO, a new D-2 agonist, was investigated in five patients with Parkinson's disease. In an acute, open, oral, dose-ranging study comparing benefit from single doses, 4 mg of PHNO was found to be equivalent to one tablet of Sinemet 25/250 mg. Adverse reactions were those anticipated for a dopaminomimetic agent. Because of its novel structure and apparent transcutaneous penetration, further studies on PHNO are desirable.