Subthalamotomy for end-stage severe Parkinson's disease.

We read with great interest the report of Alvarez and colleagues about the efficacy of subthalamotomy in advanced Parkinson’s disease. 1 While we agree that unilateral subthalamotomy has significant long-term benefits for the contralateral limbs, we are puzzled that ipsilateral limb and axial symptoms improved significantly even at the 12-month follow-up in the group of 10 Parkinson’s Disease (PD) patients with Hoehn and Yahr (H&Y) stage III–IV. Our experience has been different, as illustrated by the following case. A 64-year-old, right-handed man was diagnosed with PD in 1982 at the age of 45 years. Initial symptoms were tremor of the right hand, followed by rigidity and bradykinesia of both the right and left sides. He responded well to medications in the first 10 years of illness. He was admitted to National Taiwan University Hospital (NTUH) in April 1997 because of druginduced paranoia and pneumonia. On admission he was disoriented, there was resting tremor of the right hand, postural instability, shuffling gait, and low-volume voice. He could ambulate independently. He was discharged 12 days later with 200 mg levodopa and 50 mg benseride (Madopar; 250 mg) four times a day; Amandatine 100 mg, twice daily; Biperiden 2 mg, three times a day. He had been followed monthly at NTUH clinic since April 1997. In February 1998, he was brought to emergency room of NTUH because of severe generalized tremor and hallucination that required anti-psychotic medication, resperidone. Even with increased dosage of Madopar to five tablets per day, sometimes in addition to 100 mg of longacting levodopa and 25 mg benseride (Madopar HBS;125 mg), 1 capsule three times a day, his gait progressively worsened. He fell frequently, once resulting in a fracture of right femur neck, and was admitted to NTUH in February 98 for 14 days. Once he suffered laceration of the scalp from a fall in August 1999 that required sutures. Ever since the last fall, he had been walking with a walker. In monthly visits to NTUH clinic up until June 2000, he had been troubled with excessive salivation, choking while swallowing, drug-induced hallucinations, and gait difficulty. None of those symptoms improved despite various adjustments of medications. There has been no history of major medical problems such as hypertension, diabetes, or cardiovascular diseases. The patient was admitted to a local community hospital on July 4, 2000 because of fever, diagnosed as aspiration pneumonia. Tracheostomy was performed on August 12, 2000 because of profuse secretion that required suction hourly. Massive intravenous antibiotics were used to control pneumonia. He required tube feeding because of inability to swallow. His antiparkinsonian medication included Madopar 1,600 mg a day and Amandatine 300 mg a day with minimum benefits. He was bedridden from July 2000 to November 2000. He was transferred to the Neurology Department of NTUH on November 14, 2000 when his condition was stable after recovering from pneumonia. Evaluation in NTUH duringon state was done while he was on 1,600 mg levodopa, consisting of Madopar (250 mg) 1.5 tablets four times a day, and Madopar HBS (125 mg) four times a day. He presented with H&Y stage 5, Schwab and England scores of 10% while inon state. Unified Parkinson’s Disease Rating Scale (UPDRS) scores of activities of daily living (Part II; worst maximal score, 52) was 41 ( off) and 37 ( on). Motor examination (Part III, worst maximal scores, 108) was 104 ( off) and 88 ( on). Examination revealed tracheostomy and nasogastric tube in place. Severe rigidity, tremor and bradykinesia were present bilaterally, worse on the right side. He could not perform timed tests or finger-to-nose test with right hand due to severe rigidity and tremor. He could not turn in bed, sit up, or stand. There was prominent tremor of the face and jaw. Flexion deformity of the right and left foot was present due to severe rigidity. No lateraling weakness or sensory deficit to pinprick stimulation was present. Reflexes were 3+ bilaterally in upper and lower extremities with no Babinski sign. Magnetic resonance imaging (MRI) of brain showed no cortical atrophy, hydrocephalus or infarction. [ F]fluorodeoxyglucose (FDG)/ Positron Emission Tomography (PET) scan on November 25, 2000 after 12 hours off levodopa revealed hyperactive striatum bilaterally. The patient was placed on Amandatine up to 400 mg intravenously along with Madopar 250 mg four times a day, and Madopar HBS 125 mg four times a day, for the first 7 days while in the Neurology Department. Little improvement was noted and he continued to have hallucinations and severe tremor of the limbs, and remained bedridden. The patient was transferred to Neurosurgical service for left subthalamotomy after the risk and benefits were fully explained and accepted by him and his family. After overnight fasting and withdrawal of medication for 24 hours, a Cosman-Roberts-Wells (CRW) stereotactic frame (Radionics, Burlington, MA) was secured to the cranium of the patient under local anesthesia. A Signa 1.5-Tesla magnet (General Electric, Milwaukee, WI) MRI was used to produce 3-mmthick, nonoverlapping slices in axial, sagittal, and coronal planes. Standard T1-weighted sagittal imaging obtained parallel to the interhemispheric fissure was used to delineate the anterior commissure (AC) and posterior commissure (PC) on a midsagittal slice. Coronal T2-weighted spin echo images obtained perpendicular to the AC–PC line were used for direct visualization of the subthalamic nucleus (STN). We calculated the length of the AC–PC line and tentatively set the STN target Published online 11 March 2002 in Wiley InterScience (www. interscience.wiley.com). DOI 10.1002/mds.10130 Movement Disorders Vol. 17, No. 3, 2002, pp. 625–627 © 2002 Movement Disorder Society