worsen with fasting, cold, stretching backward, stress, and are alleviated by lightly stroking his inguinal and inframammary areas, which we interpreted as a sensory trick. He reports occasional paresthesias but denies any weakness or morning paralysis. The cramps cause mild dysphagia and shortness of breath. He denies any orthopnea, diplopia, dysarthria, or upper extrem- ity or facial involvement. He has tried muscle relaxants in the past without relief. There is no family history of neuromuscular disorders. He has had diabetes for the past 1.5 years. He has not taken any medications besides metformin. He does not drink alcohol. Mental status, cranial nerves, sensation, posture, and gait were normal. There were no signs of ocular myotonia. Motor examination of neck and extremities were 5/5 with normal tone. There were no signs of fasciculations, atrophy, muscle spasms, or percussion myotonia. Deep tendon reflexes were mildly brisk diffusely, with hyporeflexic ankle jerks and downgoing toes. CPK was normal and anti-GAD antibodies were absent. Electromyography (EMG) of the right rectus abdominis, supe- rior oblique, and external intercostals demonstrated normal motor units without any denervation potentials, myotonic dis- charges, or neuromyotonia. Applying ice and abdominal exer- cises did not provoke any abnormalities. Interestingly, motor unit recruitment was present during active (but not passive) stretching of abdominal muscles by trunk extension, suggesting co-contraction of axial muscles, supporting the diagnosis of dystonia. We prescribed clonazepam as needed, to which his symptoms had responded. To our knowledge, this is the first reported case of occupa- tional dystonia involving the truncal muscles, and that in a bricklayer. The deliberate strong, repeated contraction of ab- dominal muscles against resistance while bricklaying seems to have led to the dystonia. The EMG provided evidence of co-contraction of abdominal and axial muscles during back extension. Isolated truncal involvement has been described in tardive dystonia 1 or idiopathic primary truncal dystonia. 2 Botulinum toxin is the treatment of choice for writer’s cramp and other occupational dystonias 3 ; however, due to the widespread in- volvement, we had initially chosen an oral muscle relaxant. William Baek, MD Geoffrey Sheean, MBBS, FRACP Department of Neurology University of California San Diego San Diego, California References 1. Skidmore F, Reich SG. Tardive dystonia. Curr Treat Options Neurol 2005;7:231–236. 2. Truong DD, Sandroni P, van den Noort S, Matsumoto RR. Diphen- hydramine is effective in the treatment of idiopathic dystonia. Arch Neurol 1995;52:405– 407. 3. Karp BI. Botulinum toxin treatment of occupational and focal hand dystonia. Mov Disord 2004;19(Suppl. 8):S116 –S119. Bilateral Hemifacial Spasm and Trigeminal Neuralgia: A Unique Form of Painful Tic Convulsif Painful tic convulsif (PTC) consists of hemifacial spasm (HFS) associated to ipsilateral trigeminal neuralgia. It is a relatively rare condition, such as bilateral HFS. 1–4 We report an unusual association of bilateral HFS and trigeminal neuralgia, high- lighting the great improvement of both conditions after botuli- num toxin type A (BTX-A) therapy. A 66-year-old white male was referred to our institution with a 4-year history of bilateral facial muscle contractions. At the same time, he also noted severe electric shocklike episodic pain on the left maxillary region. He had a previous history of high blood pressure and a stroke and was taking gabapentin 800 mg/day, with partial relief of the painful sensation. On neurological examination, a bilateral hemifa- cial spasm was seen. Brain magnetic resonance imaging (MRI) disclosed an elongated and tortuous basilar artery, signs of periventricular microangiopathy and an incidental arachnoid cyst (Fig. 1). BTX-A 100 IU was injected 1 month after the first con- sultation on the left side and 52 IU on the right side. Five months later, a second injection was done. Because of cost, gabapentin was stopped and amitryptiline (50 mg/day) was prescribed. Improvement of pain was obtained after the second injection and 2 months of amitryptiline use. Bilateral hemifacial spasm also responded satisfactorily to BTX-A therapy. Bilateral involvement in HFS is very unusual and presents a challenging differential diagnosis with other neurological conditions such as facial dyskinesias, tics, cranial dystonia, and blepharospasm. 4 HFS is often attributed to vascular abnormalities nearby the facial nerve root exit zone (REZ). Mechanical compression and resultant ephaptic transmission have been considered as a cause of associated trigeminal neuralgia. 5 There is much controversy regarding the associ- ation of HFS and hypertension. The atherosclerotic arteries could compress the ventral–lateral aspect of medulla, lead- ing to a neurogenic form of hypertension. On the other hand, hypertension is known as the major cause of atherosclerosis and may hence give rise to the neurovascular abnormalities seen at the REZ of the facial nerve. 6 In our case, both ectasic basilar artery and signs of small vessel disease, together with a previous history of stroke, may indicate the association between HFS and hypertension. Once again, whether hyper- tension was cause or consequence would be merely speculative. We were not able to find any other report on the association between bilateral HFS and trigeminal neuralgia. Our case was also unusual because BTX probably improved facial twitching and pain. There is only a previous report on the association between unilateral HFS and trigeminal neuralgia with relief of the pain and facial twitching after BTX. 7 Published online 2 November 2006 in Wiley InterScience (www. interscience.wiley.com). DOI: 10.1002/mds.21202 LETTERS TO THE EDITORS 285 Movement Disorders, Vol. 22, No. 2, 2007