We set out to determine the rate of response of low-grade (WHO Grade II) gliomas to radiotherapy and analyze the relationship between radiographic response, symptom control and patient survival.

Patients were eligible for this study if they had received radiotherapy for pathologically confirmed, residual, supratentorial low-grade astrocytoma, oligodendroglioma, or mixed glioma, and imaging studies (baseline and follow-up) were available for review. Percent change in tumor size and rate and timing of response were determined by maximum linear measurement, area measurement, volume measurement using an ellipsoid model, and volume measurement by image segmentation. For each method, response to radiotherapy was defined firstly as a ≥50% decrease in tumor size (partial response), and secondly as a decrease equivalent to a 50% area decrease (normalized partial response). Relationships between radiographic response, clinical improvement and progression-free survival were analyzed using a Cox Proportional Hazard's model.

Twenty-one patients in a database (13 male, 8 female; ages 22-66 years) met the eligibility criteria. Twenty were imaged by computed tomography, 18 had an astrocytoma and 15 were irradiated soon after surgery. Responses were common and not felt to be due to a steroid effect. Use of normalized response criteria improved agreement between assessment of response as determined by the 4 methods. Median time to maximum radiographic improvement was 2.8 months (range, 1.5-11). Sixteen patients (76%) were improved neurologically, the median time to progression was 4.8 years and the 5-year progression-free survival rate was 43%. We did not detect a statistically significant association between response (as measured by any method), symptomatology and progression-free survival.

Low-grade gliomas are moderately radioresponsive. Use of volume measurement may over-estimate the number of partial responses unless a volume reduction equivalent to a 50% area decrease is used to define response. The best way to measure response remains uncertain because neither visual, area, nor volume changes confidently predicted clinical outcomes.

To determine if hypoperfusion abnormalities on single photon emission computed tomography (SPECT) are associated with poorer cognitive function at baseline or increased risk of decline in cognitive function and progression to dementia in memory-impaired but non-demented elderly subjects meeting the criteria for aging associated cognitive decline (AACD).

Cross sectional study of 36 AACD subjects comparing hexamethyl propylene-amine oxime (HMPAO) SPECT results rated by visual inspection with base line cognitive functioning. Prospective study of these AACD subjects with clinical and neuropsychological follow-up over 35 months.

The memory clinic and nuclear medicine unit of a university teaching hospital.

Thirty-six subjects meeting the criteria for AACD recruited from patients seen on a physician referral basis.

1) Baseline cognitive function as measured by the Mini Mental State Examination (MMSE), Boston naming, Logical Memory I subtest of the WAIS-R, and verbal fluency, correlated with SPECT status. 2) Decline in cognitive function as measured by clinical exam and the MMSE, with progression to dementia on follow-up being correlated with SPECT status at baseline.

18 of the 36 subjects progressed to dementia (probable Alzheimer's Disease) over follow-up. No correlation was found between the presence or absence of SPECT abnormality and MMSE or other cognitive measures. There was no correlation between the presence or absence of SPECT abnormality at initial examination, and cognitive decline according to the MMSE, or with the occurrence of clinical dementia on follow-up.

We conclude that SPECT abnormalities assessed by visual inspection do not correlate with severity of impairment in AACD individuals, and are not useful in predicting progression to dementia in AACD subjects.

Clinical experience suggests that young multiple sclerosis patients may have herpes zoster (HZ) earlier and more often than the general population. As there is evidence of a relationship between varicella zoster virus (VZV) and MS, a study of HZ and MS was undertaken.

Eight hundred and twenty-nine patient-members of the Manitoba Chapter of the Canadian Multiple Sclerosis Society were surveyed by mail. Six hundred and thirty-three (76%) responded. Questions included: age at diagnosis of MS, history of HZ (yes, no, probably), number of episodes of HZ and age at each occurrence, date of birth, and sex of respondent. The controls were consecutive patients with other neurological diseases (OND) attending local neurological or neurosurgical clinics, plus practice-based and population-based surveys of herpes zoster without reference to any other disease. The OND controls were assessed at the time of their outpatient visits.

In the MS group with a positive/probable history of HZ, the HZ/MS rate was 106/633 (16.8%); in the practice-based survey the rate was 192/3534 (5.4%); and among the patients with OND it was 42/616 (6.8%). The HZ occurred at an earlier age in the MS group. The majority of male patients had HZ prior to the diagnosis of MS. The date of diagnosis is more likely to be a precise memory as opposed to the onset of symptoms. More than one attack of HZ was also more common in the MS group.

This survey adds to the evidence that patients with MS have a unique relationship with the herpes zoster virus.

The prognostic significance of epileptiform activity (EA) recorded intraoperatively at electrocorticography (ECOG) in patients with lesion-related frontal lobe epilepsy (FLE) is unknown.

The results of ECOG performed in 22 patients with intractable FLE and a circumscribed frontal lobe structural lesion were compared with postoperative seizure control. Three patients underwent re-operation for a total of 25 cases, 23/25 with post-resection ECOG. Lesions were neoplasms (12), hamartomas (6) and arteriovenous malformations (4).

Outcomes were 15/25 Class I, 5/25 Class III and 5/25 Class IV (Engel classification). Class I outcome was associated with pre-excision EA recorded from ≤ 2 gyri (p < 0.05) and absence of EA, or EA limited to the resection border, at post-excision ECOG (p < 0.01). Complete lesion excision was highly correlated with Class I outcome (p < 0.001). The most significant correlations were seen when ECOG and lesionectomy variables were considered together: all 12 cases with complete lesionectomy and absent post-excision EA distant to the resection border had Class I outcome (p < 0.00015) and all 13 cases with complete lesionectomy and pre-excision EA recorded from ≤ 2 gyri had Class I outcome (p < 0.00005).

Postoperative seizure control in lesion-related FLE is assured in the setting of complete lesion resection with pre-excision EA recorded from ≤ 2 gyri and no post-excision EA distant to the resection border; complete lesion excision is of paramount importance.

One of the difficulties with lumboperitoneal (LP) shunts has been non-invasively ascertaining shunt function. It has been previously reported that in the presence of a functioning LP shunt the perimesencephalic cisterns become obliterated – the “absent cistern sign”. In order to more rigorously test this association we performed a retrospective analysis of LP shunt patients at the Hospital for Sick Children, Toronto.

The CT scans of all patients undergoing LP shunting over a 17 year period were reviewed. The “absent cistern sign” and ventricular size were compared against the results of either an isotope shunt study or surgical findings performed within 2 days of the CT.

There were 38 CT scans (27 patients) performed within 2 days of an isotope shunt study and 15 CT scans (14 patients) performed within 2 days of a surgical intervention. These results give the absent cistern sign a sensitivity of 75% and a specificity of 57% when compared to the shunt isotope findings and a sensitivity of 100% and a specificity of 50% when compared to the surgical findings. Over 30% of the CT scans showed ventriculomegaly in the presence of a functioning shunt and, conversely, nearly 45% of the CT scans had normal or small lateral ventricles in the presence of a malfunctioning shunt.

The “absent cistern sign” appears to reliably rule out a completely blocked shunt, but is less reliable in detecting a normal or partially obstructed shunt. Ventricular size correlates poorly with LP shunt function.

Brainstem auditory evoked potentials (BAEP) are useful indicators of auditory function during posterior fossa surgery. Several potential mechanisms of injury may affect the cochlear nerve, and complete loss of BAEP is often associated with postoperative hearing loss. We report two cases of intraoperative auditory loss related to vascular compression upon the cochlear nerve.

Intra-operative BAEP were monitored in a consecutive series of over 300 microvascu-lar decompressions (MVD) performed in a recent twelve-month period. In two patients undergoing treatment for trigeminal neuralgia, BAEP waveforms suddenly disappeared completely during closure of the dura.

The cerebello-pontine angle was immediately re-explored and there was no evidence of hemorrhage or cerebellar swelling. The cochlear nerve and brainstem were inspected, and prominent vascular compression was identified in both patients. A cochlear nerve MVD resulted in immediate restoration of BAEP, and both patients recovered without hearing loss.

These cases illustrate that vascular compression upon the cochlear nerve may disrupt function, and is reversible with MVD. Awareness of this event and recognition of BAEP changes alert the neurosurgeon to a potential reversible cause of hearing loss during posterior fossa surgery.

Cerebral venous thrombosis is a clinical entity which is readily diagnosed with the advent of modern imaging techniques. Anticoagulation is now a standard therapy, but more recent treatment strategies have included endovascular thrombolysis. While the endpoint of this intervention both clinically and radiographically has not been defined, noninvasive monitoring techniques may add further objective measures of treatment response.

We present a patient with a four day history of worsening headache and papilledema on exam. Superior sagittal, straight, and bilateral transverse sinus thromboses were identified on computed tomography and angiography.

Emergent endovascular thrombolysis by a transvenous approach re-established venous patency and resulted in immediate resolution of the patient's symptoms. Cerebral oximetry by near-infrared spectroscopy was utilized during the procedure, and changes in chromophore concentrations correlated directly with angiographic and clinical resolution of the thrombosis.

Near-infrared spectroscopy can provide continuous feedback during thrombolytic therapy in cerebral venous thrombosis and may help define endpoints of such intervention.

Perception of a phantom limb is frequent after an amputation of an upper or lower extremity. Phantom penis is reported infrequently.

Case description and literature review.

The phenomenon of phantom penis followed total penectomy. Several aspects were unusual, particularly the existence with phantom only in the erect state, and associated recrudescence of a preoperative painful ulcer. General features of limb phantoms after amputation are reviewed including a résumé of recent studies of cortical reorganization. The phantom process is analyzed looking for clues to the nature of the underlying neural organization. The puzzle of phantom pain is briefly touched on.

The development of the phantom is attributed to activity in the deafferented parietal sensory cortex.

We report an unusual case of the CT appearance of diffuse subarachnoid hemorrhage in a patient with anoxic encephalopathy, a situation which neurosurgeons, neurologists, and neuroradiologists should be aware of.

A young man collapsed unconscious in jail after abusing an unknown quantity and variety of drugs. CT scan showed a picture compatible with diffuse subarachnoid hemorrhage.

As the patient had a Glasgow Coma Score of 3 no heroic intervention was undertaken. An autopsy performed 40 hours after the initial ictus and 24 hours after death revealed no evidence of subarachnoid hemorrhage but gross and microscopic evidence of anoxic encephalopathy.

Anoxic encephalopathy can mimic diffuse subarachnoid hemorrhage on CT.

Little is known about vitamin B12 deficiency myelopathy's magnetic resonance imaging (MRI) manifestations and their relationship to the onset, evolution, and resolution of neurologic signs and symptoms.

We present a case and review eleven additional reported cases of subacute combined degeneration of the spinal cord detected by MRI.

Our patient had increased T2-weighted signal and gadolinium contrast enhancement of the posterior columns in the cervical and thoracic regions and enhancement of the lateral columns in the high cervical region. This is a case with imaging evidence for lateral column lesions. Two prior reports have shown posterior column enhancement. T1-weighted images may show decreased signal in the posterior columns and sometimes demonstrate reversible spinal cord swelling. MRI abnormalities typically improve after vitamin replacement therapy. However, clinical signs may persist despite resolution of imaging abnormalities, and these abnormalities do not always resolve completely. In addition, symptoms may precede the imaging abnormality.

Vitamin B12 deficiency may produce an increased T2-weighted signal, decreased T1-weighted signal, and contrast enhancement of the posterior and lateral columns of the spinal cord, mainly of the cervical and upper thoracic segments. Because the symptoms may precede any imaging abnormality, it is clear that spinal cord MRI may not be a highly sensitive, early test for subacute combined degeneration.