In NEUROLOGY 1995;45:753-761, a significant work followed 18 patients
who underwent pallidotomy for 12 months, at 3 month intervals
measuring motor functions. The motor functions of these patients was
compared with 7 patients who did not have the surgery.
 
The following is a synopsis:
 
Stereotactic ventral pallidotomy for Parkinson's disease
 
M. Dogali,MD;E. Fazzini,DO,PhD;E. Kolodny,MD;D. Eidelberg,MD;
D. Sterio,MD,DSc;O. Devinsky,MD; and A. Beric,MD,DSc
 
Selection: Patients with PD were selected by neurologists E. Fazzini and
E. Kolodny and neurosurgeon M. Dogali. P. PD diagnosis for this selection
was those with demonstrated parkinsonism with response to levodopa and
had no history of known causative factors such as enchepalitus or neuro-
leptic treatment.
 
Those with (1) dementia, supranuclear gaze palsy, or ataxia;(2) Stage IV
Hoehn and Yahr when "on";(3) Blood pressure drop greater than 30 mm Hg on
standing;(4) medical, neurologic, or orthopedic illness that would
compromise assessment, such as spinal stenosis, cerebrovascular disease,
or metabolic disorder; or(5) the presence of a focal brain abnormality on
MRI.
 
Patient Assessment:
 
The patients were assessed according to the "Core Assessment Program
for Intracerebral Transplantation" (CAPIT).  Surgical and non-surgical
patients were tested after being off medication for 12 Hours (12 HOM) and
several hours after waking up. Surgical patients were also tested while
in the "on" state.
 
Patients were maintained on a stable dose of antiparkinson medications
for at least 2 weeks before surgery.
 
Radiologic Investigations:
 
Magnetic resonance imaging; All patients (surgical and nonsurgical) had
T1- and T2-weighted MRI. Surgical patients had stereotactic pre- and
postoperative MRI for confirmation of lesion placement and size. Post
operative stereotactic MRIs confirmed the placement of all lesions with
+- 1 mm of preoperatively planned targets.
 
"Simplified" Surgical Procedure:
 
All patients were deprived of medications for 12 or more hours before
surgery. Under local anesthesia, a Leksell stereotactic G-frame  was affixed
at 4 points using fiberglass pins.
 
Electrical stimulation was performed before lesioning to prevent injury
to the internal capsule or optic tract; the effects and stimulation
thresholds eliciting contralateral muscle contractions or visual symptoms
were recorded.
 
Multiple lesions were made at 80 degrees C for 60 seconds. Lesions were
overlapped and created in sequence by withdrawing the electrode at 2-mm
intervals, resulting in a cylindrically shaped lesion.
 
Results:
 
All surgical patients demonstrated improvement of rigidity and bradykinesia
immediately after lesioning, while in the operating room. However, the
first formal testing was obtained 1 week after surgery. The average length
of hospitalization was 5 days, with all patients returning to their usual
activities with 10 days.
 
Lesion volume in all cases was calculated at between 60 and 90 cubic mm
with a mean of 75 mm. Ten left and 8 right pallidotomies were done.
 
There were only two events that could be considered complications. One
patient was sexually disinhibited for 24 hours after pallidotomy, which
was likely a transient effect of the surgery. The other patient suffered a
MCA stroke 7 months after pallidotomy with infarction on the side opposite
to the pallidotomy. He improved and became ambulatory with 2 to 3 months.
As his 9- and 12-month follow-ups were confounded by signs of hemiparesis,
they were excluded from the analysis; therefore, the 9- and 12-month
follow-ups are reported for 17 patients.
 
Improved reductions in test times for surgical patients were essentially
consistent from follow-up to follow-up. Non surgical patients test times
increased for the same tasks.
 
At 1 year postoperatively, eight surgical patients demonstrated an increase
in levodopa dosage or dopamine agonist use. Eight patients decreased
levodopa usage or eliminated agonists, and one patient remained on the same
medications and dosages. In contrast, five nonsurgical patients had
increased dosage, one had decreased dosage, and one remained on the same
dosage. The average levodopa dosage for surgical patients at the time of
surgery was 1,041 mg/day and at the 12-month follow-up it was 1,002 mg/day,
an insignificant 3.7% overall decrease. Pergolide dosage remained the same
in the 10 patients who used it, which is an insignificant difference despite
the tendency for decrease. Amantadine was eliminated in three of the four
patients who used it preoperatively. Apart from one patient's stopping
bromocriptine at the 12-month follow-up, no other changes were demonstrated
in the three other patients who used it.
 
Nonsurgical patients increased levodopa usage from 740 mg/day at baseline
to 977 mg/day at 12-month follow-up, a statistically significant 32%
increase.
 
No correlation was found between the age of surgical patients and degree of
improvement. Interestingly, one of the least improvements was seen in the
youngest patient and one of the best improvements was seen in one of the
oldest patients. If these two patients were excluded from the analysis,
then younger age did correlate with better outcome in the remaining 15
patients.
 
Discussion:
 
Our impression that younger PD patients showed greater improvement was
not supported by statistical analysis. We still believe that there is a real
tendency for this to occur, but due to a relatively small number of
observations as well as a few exceptions, which were alluded to in the
Results, no correlation was found. Preliminary analysis of a larger group of
postpallidotomy follow-ups, although with shorter follow-up periods, shows
that younger patients have greater improvement. However, as some older
patients enjoy considerable improvement, age should not be a relative
contraindication for pallidotomy; our oldest patient was seventy-nine.
 
Blinded review of all timed tests confirmed nonblinded clinical assessments;
there was a significant improvement in PD symptoms and signs after
pallidotomy. Patients experienced and reported improvements in overall
functioning when in their "best on" and some decrease in fluctuation of
their "on" and "off" periods; analysis of 12 HOM and "best on" improvements
confirmed those observations. In comparing the degree of change or
improvement for 12 HOM with "best on" 12 months after pallidotomy, 12 HOM
showed significantly more improvement than "best on" for all observed
parameters. Our patients were levodopa-responsive, and most had a good
response to medication except for the presence of dyskinesias during short
"on" periods. It was not expected that pallidotomy would dramatically
improve a "best on" that was already good. Large improvements in 12 HOM,
however, had to contribute to lesser fluctuations, as the "off" phase was
better after pallidotomy and scores were lower, even approaching scores
in the "on" phase.
 
Overall, there was a minimal decrease in the mean daily dosage of
antiparkinsonian medications at 12 months postoperatively as compared with
baseline. Postoperatively, the "barrier" of contralateral dyskinesia was
lifted, allowing patients to tolerate the same dosage of antiparkinsonian
medications with inducing contralateral dyskinesia.
 
Although pallidotomy may not be as effective as thalamotomy for tremor
alleviation, tremor was reduced in all affected patients. Further, speech
impairment, which is often a complication of thalamotomy, did not occur
following dominant or nondominant hemisphere pallidotomy. Also, whereas
balance impairment can be a complication of thalamotomy, pallidotomy
improved balance and ambulation as well as bradykinesia.
 
Postpallidotomy improvement appeared immediately after surgery and persisted
for the duration of the 1-year follow-up. Some additional but not
significant improvements at 1 year suggest that pallidotomy might slow the
progression of PD, because nonsurgical controls deteriorated. Such PD arrest
was suggested after some surgical interventions in the past; however,
further follow-up is necessary to confirm this observation. It is conceivable
 hat
the presence of dysfunction and hyperinhibition can further perpetuate the
imbalance and contribute to the vicious cycle of PD progression, but removal
of GPi hyperactivity may reduce the possible contribution of neuronal
circuitry hyperactivity-imbalance to the progression of PD.
 
 
 
 
 
 
 
 
John Cottingham                     [log in to unmask]