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A case of Parkinson's disease with apraxia of lid opening and freezing of gait

2011; Lippincott Williams & Wilkins; Volume: 124; Issue: 21 Linguagem: Inglês

10.3760/cma.j.issn.0366-6999.2011.21.032

2542-5641

Zhenfu Wang,

Botulinum Toxin and Related Neurological Disorders

To the Editor: The apraxia of eyelid opening (ALO) refers to a nonparalytic movement disorder of eyelid characterized by transient difficulty in voluntarily initiating the act of lid elevation in spite of preserved alertness and language comprehension.1 The typical freezing of gait (FOG) is characterized by an abrupt difficulty in starting or continuing rhythmic and repetitive movements. The frequency of ALO was 0.3%-0.7% in Parkinson's disease (PD),2,3 and it almost concurrently occurred with blepharospasm (BPS) or other dystonia. Yoon et al3 reported 3 ALO cases with BPS out of 913 PD patients. It is rare that a PD patient presents isolated ALO (not with BPS or other dystonia) as well as FOG. We reported here a case of PD with isolated ALO and FOG. A 72-year-old man with rest tremor in right hand for 10 years, difficulty in starting walking for 7 years and difficulty in opening eyes after closure for 5 years, was admitted to our department. Two years after onset of rest tremor in right hand, the patient showed rest tremor in left hand, hypokinesia and mild rigidity, diagnosed as PD. After another year, he felt difficult in starting walking of legs, trembled in place and then walked normally, but trembled in place again while entering a narrow door or turning round and somebody said hello to him, he showed a walk way of repetitive standing with trembling/walking. Five years after the onset, the patient felt difficult in opening eyes after voluntary closure. There was no BPS and other types of distonia. In recent several months, ALO and FOG kept him closing eyes and sitting almost all day, they were not improved while the patient took antiparkinsonism drugs (very low doses). It helped him open eyes to put his fingers on upper eyelids, and external cueing, treadmill exercise and striding over an object (the patient tied a piece of wood, thrown it before his feet, then strode over it and started walking) could alleviate FOG. Eleven years after the onset, the ALO and FOG became more severe, but parkinsonism showed a little change. Neurological evaluation showed normal function besides ALO, FOG, parkinsonism and excessive wrinkling of fore head while the patient attempted to open his eyes, which showed over action of frontalis. Plain brain MRI scanning was normal. Goldstein and Cogan1 first coined the term of ALO. Patients feel difficulty in initiating the act of lid elevation with which they do not have true ptosis but have difficulty in overcoming levator palpebrae inhibition or/and pretarsal orbicularis oculi muscle (OO) persistent contraction while opening their eyes. There is clinically no overt spasm of the OO and the eyes appeared to be passively shut with frontalis muscle overaction causing elevation of the brows. Tricks may be used to help open the eyes. We diagnosed ALO according with Lepore and Duvoisin's commonly accepted clinical criteria.4 It is most commonly seen when there were lesions in the periventricular or peristriatal white matter that involve association fibres, in particular those of the superior longitudinal fasciculus and frontostriatal connections.5 Recently ALO has been reported in up to 31% of patients undergoing subthalamic nucleus deep brain stimulation for PD.6 But Goto et al7 reported ALO was alleviated by pallidal DBS in a PD patient with ALO as well as FOG. The FOG is a motor symptom of PD with which patients feel their feet becoming "glued to the floor". The trembling in place is actually the most common presentation,8 that patients try to overcome the block causing their legs to tremble in place, especially when patients initiate walking or turn, cross narrow spaces, reach a target or an obstacle. It is thought of one kind of "frontal gait disorder", occurring when damage to white matter tracts alters communication between the basal ganglia and the supplementary motor area. FOG is usually regarded as a "late" feature of PD that is independent on akinesia, occurs more frequently in the subgroup of PD with the akinetic form and is a clinical marker for more rapid disease progression and reduced survival. This case showed mild hypokinesia that made clear the FOG was not dependent on akinesia, lack of the common features of PD patients with FOG and a slow progression of parkinsonism. There is a clinical similarity between ALO and FOG, and they both involve in disturbed communication between the basal ganglia and the frontal lobe.