The treatment of unruptured, intracranial aneurysms has been the topic of debate. Although recent studies have advocated surgical intervention for unruptured aneurysms, the risk of such treatment in comparison to outcome from ruptured aneurysms has not been established.

This retrospective study examines the outcome of 134 patients with 179 ruptured and unruptured intracranial, saccular aneurysms treated by a single surgeon.

Of the 98 ruptured aneurysms where early surgical intervention was undertaken (less than 48 hours post hemorrhage), 70 had an excellent outcome, 13 were good, four were moderate, two poor and nine patients died postoperatively. Outcome assessment in these cases was correlated to preoperative neurological status. Patients who presented with unruptured aneurysms fell into two categories: symptomatic and asymptomatic. Seven incidental, asymptomatic aneurysms were clipped concurrently to the surgical isolation of the culprit lesion following subarachnoid hemorrhage without influencing outcome, whilst, for varying reasons, eight unruptured aneurysms were not operated upon. Of the remaining 66 surgically treated, unruptured aneurysms, 64 had an excellent postoperative result, one was good (persisting right incomplete third nerve palsy) and one was moderate (left hemiparesis). Thirteen of these aneurysms were symptomatic, whilst 21 were asymptomatic, multiple aneurysms requiring secondary elective repair and 32 were true incidental aneurysms.

Unruptured aneurysms less than 25 mm in size may be safely, surgically treated relative to the expected natural history and, certainly, with less risk than operative intervention upon ruptured cerebral aneurysms.

Despite the potential importance of endoneurial microvessel abnormalities in diabetic neuropathy, the pathogenesis of these abnormalities is incompletely understood. We wished to evaluate the effect of experimental diabetes on endoneurial microvessels and determine if an aldose reductase inhibitor alters any of the changes induced by diabetes.

We compared streptozocin diabetic rats with and without aldose reductase inhibitor treatment to non-diabetic rats after 10 months of diabetes. Transverse microvessels from the mid-sciatic level were studied by electron microscopic morphometric evaluation.

Microvessel endothelial, pericyte, basement membrane and total mural area were greater in untreated diabetic animals than non-diabetic animals. Aldose reductase inhibitor treated diabetic animals had greater endothelial area and possibly pericyte area but not basement membrane or total mural area.

This study demonstrates that endoneurial microvessel abnormalities can be detected in experimental diabetic neuropathy. Microvessel basement membrane thickening will be prevented by an aldose reductase inhibitor. One mechanism by which abnormal polyol pathway activity may contribute to diabetic neuropathy could be through damage to microvessels.

In two previous studies we have demonstrated prevention of electrophysiological abnormalities of nerve in experimental STZ (streptozotocin)-induced diabetes (ED) of rats using nonsteroidal anti-inflammatory agents: indomethacin and sulindac. Sulindac might benefit ED because it inhibits both cyclo-oxygenase and aldose reductase.

In this work, we examined whether 1 month of sulindac treatment reversed or improved established biochemical and electrophysiological abnormalities in experimental diabetes of 3 months duration. Sulindac-treated diabetic rats (6.0 mg/kg 5/7 days weekly by gavage) were compared to untreated diabetics, nondiabetic controls and sulindac treated control rats.

Diabetic rats developed slowing of conduction velocity in caudal sensory, sural sensory, caudal motor and sciatic tibial motor fibers. Sulindac improved caudal motor and, to a lesser extent sural sensory conduction but not caudal sensory or sciatic tibial motor conduction. Sulindac did not alter sciatic sugars or polyols.

Sulindac provided modest improvement in some indices of experimental neuropathy in this reversal study, but there was less efficacy than in the preventative study. Reversal paradigms should be examined in all experimental therapies for diabetic neuropathy.

As in the brain, recent evidence has suggested a defect in the microcirculation during the reperfusion period after spinal cord ischemia. This investigation was undertaken in order to delineate blood flow dynamics in the postischemic spinal cord of the rat.

Male Sprague-Dawley rats underwent cross-clamping of the aorta and subclavian arteries (XC) for 11 minutes. Spinal cord blood flow (SCBF) was measured by autoradiography in the gray and white matter of cervical (Ce), thoracic (Th) and lumbar (Lu) regions during XC, 1 h, 6 h and 24 h (XC n = 8, 1 h n = 9, 6 h n = 9, and 24 h n = 11, groups) after XC. Control groups underwent surgical manipulations and SCBF measurement but no XC (Sham 1, n = 8), or clamping of the subclavian arteries only (Sham 2, n = 8).

In Ce cord, there was no difference between SCBF of 1 h, 6 h, 24 h and Sham 1. In Th cord, SCBF was reduced during XC (P < 0.003 vs. Sham 2), 1 h, 6 h (P < 0.04 and P < 0.01 vs. Sham 1). In Lu cord, SCBF was not detectable in XC, and depressed in 1 h (P < 0.003) and 6 h (P < 0.003). There was no difference between 24 h and Sham 1 in Ce, Th, and Lu cords.

The study demonstrated a period of delayed postischemic hypoperfusion in the white and gray matter of Th and Lu cord segments lasting 6 h after XC. The phenomenon may play an important role in the ultimate fate of neural elements with borderline viability after ischemic injury.

Severe spasticity unresponsive to oral drugs may respond satisfactorily to baclofen delivered intrathecally.

Intrathecal baclofen (IB) therapy delivered by means of implanted infusion pumps was used for nine patients with severe spasticity. Six patients had multiple sclerosis, two cervical spinal cord injury, and one head injury. All were non-ambulatory.

Patients showed improvement in many areas, including ability to transfer, seating, pain control, personal care, and liability to skin breakdown. Before IB therapy, only three of the nine patients were able to live at home in the community and six were institutionalized. At the end of our follow-up period, only one patient remained institutionalized, three lived in group homes and five lived at home in the community. In the year preceding pump implantation, the nine patients spent a total of 755 days in acute care hospitals. In the year following onset of IB therapy, they spent only 259 days in hospital.

IB therapy can improve patient quality of life and can be cost-effective in carefully selected patients with severe spasticity and disability. The drug delivery catheter is that part of the therapeutic system most vulnerable to failure. Because of the varied expertise required to manage these patients effectively, and the potential for a variety of complications, it is essential that an IB program is supported by a well-organized multi-disciplinary medical team.

We tested the effect of thiopental on the excitability of the corticospinal-motoneuron axis in normal human subjects.

Magnetic stimulation was used to excite the neurons in the motor cortex which give rise to the fast conducting corticospinal pathway. The characteristics of the composite excitatory post-synaptic potentials (EPSPs) produced in individual spinal motoneurons by cortical stimulation were derived from changes in the firing probability of voluntarily activated motor units of the first dorsal interosseous muscle.

In 5 normal subjects, we found that thiopental, in incremental doses sufficient to sustain drowsiness (total dose 75 to 175 mg), significantly reduced the amplitude of these composite EPSPs.

Thiopental reduced the facilitation of motoneurons from the cortex most likely by depressing cortical neurons.

One of the major symptoms of postpoliomyelitis syndrome (PPS) is disabling generalized fatigue. Subjects with PPS also report muscle fatiguability and display electrophysiologic evidence of anticholinesterase-responsive neuromuscular junction transmission defects, suggesting that anticholinesterase therapy may be useful in the management of disabling fatigue.

We initiated an open trial of the oral anticholinesterase pyridostigmine, up to 180 mg per day, in 27 PPS patients with generalized fatigue and muscle fatiguability. Response to pyridostigmine was assessed with the Hare fatigue scale, the modified Barthel index for activities of daily living, and a modified Klingman mobility index.

Two patients could not tolerate the medication. After one month of therapy, 16 patients (64%) reported a reduction in fatigue on the Hare fatigue scale; three of 16 showed improvement on the modified Barthel index for activities of daily living, and two of 16 experienced improvement on a modified Klingman mobility index. Pyridostigmine responders were significantly more fatigued than non-responders on the pre-treatment Hare score, but were not significantly different with regard to age, sex, age at acute poliomyelitis, or severity of acute poliomyelitis.

Pyridostigmine may be useful in the management of fatigue in selected patients with PPS. Response to pyridostigmine may be predicted by severity of pre-treatment fatigue.

Multiple Sclerosis (MS) is associated with a high risk of developing major depression, but depression in MS patients frequently goes undetected and untreated. The current study examined the clinical utility of the Beck Depression Inventory (BDI) as a screening measure for major depression in newly diagnosed MS patients.

Forty-six new referrals to an MS clinic completed the BDI and participated in a structured interview for major depression, within 2 months of the diagnosis of MS.

According to DSM-III-R criteria, 40% of patients were diagnosed with major depression, 22% had adjustment disorder with depressed mood, and 37% showed no evidence of mood disorder. Sensitivity and specificity values, and positive and negative predictive values are reported for every BDI cut-off score between 9 and 21.

A BDI cut-off score of 13 (sensitivity = .71, specificity = .79) is recommended as optimal for use in screening for major depression in newly diagnosed MS patients. The use of the BDI as a screening measure for major depression must proceed with caution given that a cut-off score of 13 still yielded a false-negative rate of 30%.

Etiologic hypotheses for Parkinson’s disease have implicated environmental factors, genetic factors, or a combination of the two.

Data from a survey of elderly Canadians (n = 10,263) with regard to their history of Parkinson’s disease and previous environmental exposures were analyzed. Exposure to various environmental factors was compared between 87 patients with Parkinson’s disease and 2070 elderly controls without Parkinson’s disease.

Exposure to plastic resins (OR (odd ratio) = 8.79), epoxy resins (OR = 6.94), glues (OR = 4.26), paints (OR = 3.84), and petroleum (OR = 2.30) products was significantly (p < 0.05) associated with Parkinson’s disease.

These substances deserve further exploration with respect to the possible development of parkinsonism.

Stereotactic insertion of catherters into deep-seated tumors or developmental cysts is easily accomplished, but connecting the catheter to an Ommaya reservoir while maintaining catheter position can be difficult. We describe a technique for easy placement of a catheter-Ommaya reservoir construct with one pass.

Standard stereotactic imaging is performed. The distance from the outer table of the skull to the target point is measured. A catheter-Ommaya reservoir construct is assembled to this length and directed to the target position with a standard Cosman-Robert-Wells (CRW) stereotactic frame.

Use of this technique placed catheters into tumor or developmental cysts accurately and with no surgical complications in 12 patients.

This technique is simple, safe, reliable, and requires no special equipment. It avoids the risk of dislodging the catheter when it is being connected to the Ommaya reservoir, reducing the chances of cyst leakage and collapse.

Progressive deterioration and ensuing death following a neurosurgical procedure often represents a diagnostic challenge to the team responsible for patient care. Many, but not all, causes are treatable if a diagnosis is made early.

A 69-year-old woman who died 6 weeks post-operatively following a meningioma resection is reported. An initial routine post-operative course became complicated by progressive neurological deterioration 3–4 weeks later. Despite extensive investigation she died 6 weeks post-operatively without a diagnosis.

Autopsy demonstrated extensive Candida meningitis. A review of the literature demonstrates this to be a reported complication in high risk patients, difficult to diagnose, but treatable when identified.

Fungal meningitis should be high in the differential diagnosis in the post-operative patient with delayed, unexplained neurological deterioration, especially when associated with negative CSF cultures.

Neuroleptic Malignant Syndrome (NMS) is an adverse reaction to dopamine receptor antagonists, characterised by hyperpyrexia, extrapyramidal rigidity and impaired autonomic function. It might result from central dopamine receptor blockade that causes severe muscle contraction.

Case Study.

High dose intravenous therapy with the anticholinergic drug, procyclidine hydrochloride, temporarily diminished the muscle rigidity and reversed most of the autonomic features in a patient with NMS occurring after a single intramuscular dose of the dopamine antagonist metoclopramide. Paradoxically, however, the heart rate decreased and bowel movements increased with this atropine-like drug.

Since the degree of tachypnoea, tachycardia, and bowel hypotonia closely paralleled the severity of the muscle rigidity, it is suggested that these autonomic features of NMS result from sustained muscle contraction rather than a direct effect of neuroleptic drugs on the central nervous system.