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Background: Brain size has been associated with intelligence of various orders and families of animals, leading to the concept of encephalization. Brain size scales with body weight between species within mammals to approximately the 0.67 power. However, within species, this scaling exponent appears to be much smaller (approximately 0.27 power)., Aim: We examined whether this relationship has persisted in dogs over the 120 years since this was originally observed., Methods: Comparative cross-sectional study of magnetic resonance imaging (MRI) data obtained from 127 dogs, compared to historical data from 157 dogs and 24 non-dog canid species., Results: Brain size in dogs measured by MRI had a scaling exponent virtually identical to that observed previously (0.24 vs. 0.26). However, the proportionality constant was smaller, suggesting that dogs in the study cohort had relatively smaller brains than the historical cohort. Absolute brain size appeared to have both a lower and upper limit in dogs. When compared to non-dogs canids, the most appropriate "representative" size for a "typical dog" when examining allometric scaling across Canidae appeared to be approximately 10-15 kg., Conclusions: We interpreted the slight reduction in relative brain size to be a function of increased obesity in the study cohort compared to dogs examined 120 years ago. Further, we suggest that dog brains have a finite lower size limit. Finally, concepts of encephalization should not be applied to dogs., Competing Interests: The authors have no conflicts of interest to declare.

Objective: To objectively describe morphometric features of the craniocervical junction region of Cavalier King Charles Spaniels (CKCSs) and non-CKCS dogs with suspected Chiari-like malformation (CLM) and identify associations between these features and the presence of other malformations in this region., Animals: 216 CKCSs and 58 non-CKCS dogs., Procedures: Magnetic resonance and computed tomographic images of the head and craniocervical junction region of patients evaluated because of suspected CLM were assessed for cerebellar compression (CC), ventral spinal cord compression at the C1-C2 articulation (medullary kinking), and dorsal spinal cord compression at the C1-C2 articulation (dorsal compression). A compression index was calculated for each of these 3 locations in each dog. Multiple logistic regression analysis was performed to determine whether breed (CKCS vs non-CKCS) and compression index values were associated with the presence of other craniocervical junction abnormalities., Results: All 274 dogs had CC; medullary kinking was identified in 187 (68.2%) and dorsal compression was identified in 104 (38.0%). Atlantooccipital overlapping (AOO) was identified in 76 (27.7%) dogs. Breed of dog (CKCS vs non-CKCS) and value of CC index were the only significant predictors of AOO. The CKCSs had an almost 5-fold decrease in risk of AOO, compared with the non-CKCS dogs, and the risk of AOO nearly doubled for every 10% increase in CC index., Conclusions and Clinical Relevance: The anatomic abnormality responsible for CC was AOO in a substantial percentage of dogs suspected to have CLM. The CC index value may be used to help differentiate subtypes of craniocervical junction abnormalities in dogs.

Objective: To describe the pharmacokinetics of pregabalin in normal dogs after a single oral dose., Study Design: Prospective experiment., Animals: Six adult Labrador/Greyhound dogs (four females and two males) aged 2.6 (2.6-5.6) years old (median and range) weighing 33.4 (26.8-42.1) kg., Methods: After jugular vein catheterization, the dogs received a single oral dose of pregabalin ( approximately 4 mg kg(-1)). Blood samples were collected at: 0 (before drug administration), 15 and 30 minutes and at 1, 1.5, 2, 3, 4, 6, 8, 12, 24 and 36 hours after drug administration. Plasma pregabalin concentration was measured by HPLC. Noncompartmental analysis was used to estimate pharmacokinetic variables., Results: No adverse effects were observed. The median (range) pharmacokinetic parameters were: Area under the curve from time 0 to 36 hours = 81.8 (56.5-92.1) microg hour mL(-1); absorption half-life = 0.38 (0.25-1.11) hours; elimination half-life = 6.90 (6.21-7.40) hours; time over 2.8 microg mL(-1) (the presumed minimal effective concentration) = 11.11 (6.97-14.47) hours; maximal plasma concentration (C(max)) = 7.15 (4.6-7.9) microg mL(-1); time for C(max) to occur = 1.5 (1.0-4.0) hours. Assuming an 8-hour dosing interval, predicted minimal, average, and maximal steady state plasma concentrations were 6.5 (4.8-8.1), 8.8 (7.3-10.9), and 13.0 (8.8-15.2) microg mL(-1). The corresponding values assuming a 12-hour interval were 3.8 (2.4-4.8), 6.8 (4.9-7.9), and 10.1 (6.6-11.6) microg mL(-1)., Conclusions and Clinical Relevance: Pregabalin 4 mg kg(-1) PO produces plasma concentrations within the extrapolated therapeutic range from humans for sufficient time to suggest that a twice daily dosing regime would be adequate. Further study of the drug's safety and efficacy for the treatment of neuropathic pain and seizures in dogs is warranted.

A 3-year-old male neutered Pomeranian presented with severe, poorly localizable pain that was unresponsive to a combination of oral medications (gabapentin, tramadol, prednisone, and methocarbamol) and a fentanyl patch. A Chiari-like malformation with associated syringomyelia was evident on magnetic resonance imaging (MRI). In addition, overlapping of the dorsal arch of C1 and the dorsal aspect of the foramen magnum was suspected from the MRI scans and verified via computed tomography, suggesting a condition similar to basilar invagination/impression in people. At surgery, a combination of foramen magnum decompression with cranioplasty and stabilization of the atlanto-occipital junction was performed. The atlanto-occipital junction was stabilized using an adaptation of a procedure used in people for basilar invagination/impression. Over the next several months, the dog's clinical signs improved dramatically, allowing substantial reduction of oral pain medications. This is the first report of surgical stabilization for atlanto-occipital overlapping in a dog.

The imaging features of four dogs with atlanto-occipital overlapping are described. This malformation appeared to play a role in the development of neck pain, ataxia, variable cerebellar involvement, medullary kinking, and possibly syringomyelia. Using cervical radiographs, three of the four dogs were initially diagnosed with an atlanto-axial malformation. Because this disorder could not account for all clinical signs, magnetic resonance and computed tomography images were also acquired. These provided a more complete evaluation of the craniocervical junction, allowing detection of atlanto-occipital overlapping, medullary kinking, occipital dysplasia, abnormalities of the dens, and syringomyelia in these dogs. Head position during imaging affected the degree of atlanto-occipital overlap. These findings emphasize the need to modify the currently accepted imaging recommendations for dogs with head and neck pain and/or cranial cervical myelopathy. We suggest that the entire craniocervical junction be evaluated, even if atlanto-axial subluxation has already been detected. Moreover, we propose that atlanto-occipital overlapping is a perhaps underrecognized disorder that can influence the clinical signs and therapeutic outcome of dogs with anomalies of the craniocervical junction.

Objectives: To describe a cranioplasty procedure used in conjunction with foramen magnum decompression (FMD) for the treatment of canine caudal occipital malformation syndrome (COMS), and to evaluate the clinical outcome., Study Design: Prospective clinical study., Animals: Dogs (n=21) with COMS diagnosed by magnetic resonance imaging (MRI)., Methods: After FMD, titanium screws were placed around the perimeter of the foramen magnum defect and a skull plate fashioned from titanium mesh and polymethylmethacrylate was attached to the back of the skull, using the titanium screws as anchor posts. Follow-up was obtained by direct examination by the authors, telephone interviews with owners and referring veterinarians, and a questionnaire sent to owners of surviving dogs designed to assign objective measures of response to surgical intervention. Surgical success was defined as improvement in >or=1 aspects of clinical dysfunction (e.g. scratching, pain) postoperatively. Owner-assigned pre- and postoperative quality-of-life (QOL) scores (1-5) for surviving dogs were compared using a Wilcoxon's signed rank test for paired data (P

A method for foramen magnum decompression (FMD) in dogs with caudal occipital malformation syndrome (COMS) and results for 16 dogs are described. In brief, a dorsal approach to the caudal portion of the occiput and arch of the atlas was made, and a high-speed drill was used to remove a portion of the occiput in the region of the foramen magnum and the dorsal aspect of C1. The meninges that were exposed were removed or marsupialized to surrounding tissues. Foramen magnum decompression was performed in 16 dogs. No intraoperative complications occurred, and postoperative complications occurred in only 2 dogs after initial surgery and in 1 of these dogs after follow-up surgery. In both dogs, postoperative complications after the initial surgery resolved without additional treatment. One dog was nonambulatory tetraparetic after follow-up surgery and died of a suspected ruptured viscus 9 days after surgery. Four dogs developed evidence of scar formation at the surgery site and required additional surgery. Overall, 14 dogs survived, 1 died, and 1 was euthanatized. Clinical signs resolved in 7 of the 14 dogs that survived, improved in 6, and did not change in 1. Results suggest that FMD may be an effective treatment for dogs with COMS, especially if performed early in the course of the disease.

Background: Canine cognitive dysfunction (CCD) is considered the canine version of human Alzheimer's disease (AD). As with AD, CCD is a multifactorial and progressive neurodegenerative disorder for which effective treatment options are continuously being sought. Transcranial photobiomodulation (tPBMT) or transcranial laser therapy has shown promise as a treatment for cognitive impairment in rodent AD investigations and several human AD clinical trials. Aim: The purpose of this prospective case series was to evaluate the effect of tPBMT on cognitive scores when applied to senior dogs with CCD over a 60-day period. Methods: Five senior (>9-year-old) dogs with moderate (16-33) to severe (>33) cognitive scores were enrolled. Owners were instructed on the use of a Class IM laser device and administered a specific dose of laser energy transcranially to both sides of the patient's head, three times per week for one month and two times per week for a second month. No additional therapeutic measures aimed at enhancing cognitive ability were permitted during the 60-day evaluation time. Baseline cognitive scores were compared with scores obtained at 30- and 60-days post-treatment. Results: Cognitive scores showed improvement in 4/5 dogs at 30 days (27.6% reduction) and all dogs at 60 days (43.4% reduction). There were no adverse effects attributable to tPBMT. Conclusion: Results of our small case series suggest that tPBMT may improve cognitive scores in dogs with moderate to severe CCD by 30 days of application and the improvement is sustained at 60 days. Further studies are needed to ascertain optimal tPBMT protocols for CCD. [ABSTRACT FROM AUTHOR]

Background: Canine cognitive dysfunction (CCD), the dog analog of human Alzheimer's disease (AD), is a progressive neurodegenerative condition that presents many treatment challenges. There are few effective drugs with acceptable side effects for AD/CCD, which has prompted investigation into non-drug options, collectively termed nutraceuticals. Nutraceutical supplements are conceptually divided into conventional (Western) and non-conventional (Eastern) ingredients. Many of these individual supplements have shown in vitro and/or in vivo efficacy in ameliorating neuronal damage in rodent models, and some have demonstrated positive effects on cognition in rodent models and clinical trials in dogs and humans with cognitive impairment. Aim: The purpose of this open-label clinical trial was to investigate the effect of an oral integrative (combination of conventional nutraceuticals and Chinese herbals) supplement (CogniCaps®) on cognitive scores when administered to aging dogs with CCD over a 2-month period. Methods: Ten aging (>9-year-old) dogs with moderate (16-33) cognitive scores were recruited and administered oral CogniCaps® for two months. No additional drugs or nutraceuticals directed at improving cognitive function were allowed during the study period. Baseline cognitive scores were compared with those procured at 30 and 60 days. Cognitive scores for baseline, 30- and 60-days post-treatment were compared. Results: Cognitive scores improved at 30 days (38% reduction) and 60 days (41% reduction) post-treatment (p = 0.002). Scores did not differ between 30- and 60-day assessments (p = 0.7). Conclusion: The results of this small preliminary study suggest that the integrative supplement CogniCaps® might improve cognitive scores in dogs with CCD within the first 30 days of administration and that this improvement is sustained at 60-day follow up. [ABSTRACT FROM AUTHOR]

Background: Idiopathic or genetic epilepsy commonly affects dogs; affected dogs are often refractory to anti-seizure drug therapy. Felbamate is an anti-seizure drug with established pharmacokinetic and safety data for dogs, but little published evidence of efficacy for managing generalized seizures in this species. Aim: The purpose of this retrospective case series was to evaluate the clinical efficacy and tolerability of oral felbamate in six presumptive epileptic dogs experiencing generalized seizures. Methods: Medical records from six dogs with presumptive idiopathic/genetic epilepsy manifesting as generalized seizure activity, for which oral felbamate was used as an add-on treatment, were reviewed. The number of seizures recorded for the 3-month period immediately before instituting felbamate was recorded for each dog. Short-term (3 months) and long-term (6 months or greater) seizure frequency post-felbamate therapy was recorded for each dog and compared with baseline. Results: Overall, dogs experienced a reduction (82%) in seizures after adding felbamate in the short term, with 5/6 dogs (83%) classified as responders (50% or greater reduction in seizures) and 3/6 dogs (50%) attaining seizure-free status. Mean and median long-term follow-up times were 13 and 11 months, respectively (range: 6 to 23 months). Four of the 6 dogs (67%) remained drug responders at final follow-up, with an average seizure reduction of 98%, 2 of which remained seizure-free at 8 and 21 months. Two dogs (33%) experienced increased seizure activity during long-term follow-up (12 and 23 months) and were considered non-responders. The non-responder dogs had an average long-term seizure reduction of 33%. No dog experienced any obvious adverse effects associated with felbamate administration. However, one dog not included in the analysis because of insufficient (<3 month) post-felbamate follow-up, was weaned off felbamate because of suspected hepatotoxicity. Conclusion: Our small case series suggests that oral felbamate might show promise as an add-on drug for epileptic dogs experiencing generalized seizures resistant to drug therapy. These results warrant a more controlled, prospective investigation into felbamate as a therapeutic agent for canine epilepsy. [ABSTRACT FROM AUTHOR]

Background: Periodontal disease has been linked to the development of Alzheimer's disease in people. It is theorized that the chronic inflammatory condition characteristic of oral dysbiosis in patients with periodontal disease leads to disruption of the blood--brain barrier, cytotoxin- and pathogen-induced brain damage, and accumulation of neurotoxic β-amyloid. In this inflammatory theory of Alzheimer's disease, β-amyloid--a known antimicrobial protein--accumulates in response to oral pathogens. Canine cognitive dysfunction (CCD) is considered a naturally occurring animal model of human Alzheimer's disease. Like humans, periodontal disease is quite common in dogs; however, a link between periodontal disease and cognitive dysfunction has not been identified in this species. Aim: The purpose of this prospective investigation was to compare visual periodontal scores (from digital oral photographs) with numerical (0--54) cognitive assessment questionnaire forms in aging dogs with and without a clinical diagnosis of CCD. Methods: A visual analogue scale (0--4) was used to score the severity of periodontal disease in 21 aging dogs: 11 dogs with a clinical diagnosis of presumptive CCD and 10 dogs without a clinical history of cognitive decline. Individuals scoring the dental photographs were blinded to all case information, including cognitive assessment scores. Cognitive assessment scores were compared with periodontal disease scores for all dogs. Results: There was a significant (p < 0.05) association between periodontal and cognitive scores, with higher cognitive impairment scores being more likely in dogs with more severe periodontal disease and vice versa. No associations were identified between age and either periodontal disease or cognitive impairment. Conclusion: Although a cause-and-effect relationship between periodontal disease and cognitive impairment cannot be ascertained from this preliminary study, we established a link between these two disorders that warrants further investigation using more stringent criteria for evaluating both periodontal disease and cognitive dysfunction. [ABSTRACT FROM AUTHOR]

Background: Degenerative myelopathy (DM) in dogs is a progressive neurodegenerative condition that causes white matter spinal cord lesions. These lesions are undetectable on standard magnetic resonance imaging (MRI), limiting diagnosis and monitoring of the disease. Spinal cord lesions cause disruption to the structural integrity of the axons causing water diffusion to become more random and less anisotropic. These changes are detectable by the technique of diffusion tensor imaging (DTI) which is highly sensitive to diffusion alterations secondary to white matter lesion development. Objective: Perform spinal DTI on cohorts of dogs with and without DM to identify if lesions caused by DM will cause a detectable alteration in spinal cord diffusivity that correlates with neurological status. Animals Thirteen dogs with DM and 13 aged‐matched controls. Methods: All animals underwent MRI with DTI of the entire spine. Diffusivity parameters fractional anisotropy (FA) and mean diffusivity (MD) were measured at each vertebral level and statistically compared between groups. Results: Dogs with DM had significant decreases in FA within the regions of the spinal cord that had high expected lesion load. Decreases in FA were most significant in dogs with severe forms of the disease and correlated with neurological grade. Conclusions and Clinical Importance: Findings suggest that FA has the potential to be a biomarker for spinal cord lesion development in DM and could play an important role in improving diagnosis and monitoring of this condition. [ABSTRACT FROM AUTHOR]

Background: Hippocampal atrophy is a key pathologic and magnetic resonance imaging (MRI) feature of human Alzheimer's disease (AD). Hippocampal atrophy has not been documented via MRI in canine cognitive dysfunction (CCD), which is considered as the dog model of human AD. Aim: The purpose of this retrospective comparative volumetric MRI study was to compare total hippocampal volumes between successfully aging (control) dogs and dogs diagnosed with CCD. Methods: Mimics® software was used to derive total hippocampal volumes and total brain volumes from the MRI studies of 42 aging dogs (= 9 years): 16 dogs diagnosed with CCD and 26 successfully aging controls. Hippocampal volumes were normalized to total brain volume and these values were compared between groups using Mann-Whitney U tests. Results: Total hippocampal volume normalized to total brain volume was significantly less for CCD patients compared with control dogs (p = 0.04). Conclusion: The results of this study suggest that - similar to human AD - hippocampal atrophy is a pathological feature of CCD. This finding has potential importance for both investigating disease mechanisms related to dementia as well as future hippocampal-targeted therapies. [ABSTRACT FROM AUTHOR]

Objective: Spontaneous brain microhemorrhages in elderly people are present to some degree in Alzheimer’s disease patients but have been linked to brain atrophy in the absence of obvious cognitive decline. Brain microhemorrhages have recently been described in older dogs, but it is unclear whether these are associated with brain atrophy. Diminution of interthalamic adhesion size-as measured on MRI or CT-has been shown to be a reliable indicator of brain atrophy in dogs with canine cognitive dysfunction (CCD) in comparison with successfully aging dogs. We hypothesized that aging dogs with brain microhemorrhages presenting for neurologic dysfunction but without obvious features of cognitive decline would have small interthalamic adhesion measurements, like dogs with CCD, compared with control dogs. The objective of this study was to compare interthalamic adhesion size between three groups of aging (>9 years) dogs: (1) neurologically impaired dogs with presumptive spontaneous brain microhemorrhages and no clinical evidence of cognitive dysfunction (2) dogs with CCD (3) dogs without clinical evidence of encephalopathy on neurologic examination (control dogs). MR images from 52 aging dogs were reviewed and measurements were obtained of interthalamic adhesion height (thickness) and mid-sagittal interthalamic adhesion area for all dogs, in addition to total brain volume. Interthalamic adhesion measurements, either absolute or normalized to total brain volume were compared between groups. Signalment (age, breed, sex), body weight, presence and number of SBMs, as well as other abnormal MRI findings were recorded for all dogs. Results: All interthalamic adhesion measurement parameters were significantly (P < 0.05) different between control dogs and affected dogs. Both dogs with cognitive dysfunction (12/15; 80%) and dogs with isolated brain microhemorrhages had more microhemorrhages than control dogs (3/25; 12%). Affected dogs without cognitive dysfunction had significantly more microhemorrhages than dogs with cognitive dysfunction. In addition to signs of cognitive impairment for the CCD group, main clinical complaints for SBM and CCD dogs were referable to central vestibular dysfunction, recent-onset seizure activity, or both. Geriatric dogs with spontaneous brain microhemorrhages without cognitive dysfunction have similar MRI abnormalities as dogs with cognitive dysfunction but may represent a distinct disease category. [ABSTRACT FROM AUTHOR]

Objective: Reports of cerebellar infarction in veterinary literature are rare. Documentation and descriptions of cerebellar infarction in human literature have been well described. Brain lesions suspected to be infarcts have been recognized with magnetic resonance imaging (MRI). Series summary: Four dogs presented to the Long Island Veterinary Specialists (LIVS) with the history of acute onset cerebellovestibular dysfunction. All animals were imaged using a 0.5 T super-conducting Magna GE MRI unit. Suspected cerebellar infarction was diagnosed in all dogs based on history, physical examination, and MRI findings. Further diagnostics were performed based on the individual case and owner compliance. Functional recovery was favorable in 3 dogs. One dog was euthanized shortly following the onset of neurological dysfunction. New or unique information provided: Cerebellar infarction appears to have characteristic MRI features. Affected tissue within the cerebellum is typically wedge-shaped with low signal intensity in T1-weighted images, high signal intensity in T2-weighted images, subtle rim enhancement without central contrast enhancement in T1 post-gadolinium, and selectively hyperintense in fluid-attenuated inversion recovery images. Anatomic regions serviced by rostral cerebellar arteries are affected. Vascular risk factors as compared with reports in human literature are also discussed. [ABSTRACT FROM AUTHOR]

Presents the abstract of the case study "Vascular Encephalopathy Associated With Bacterial Endocarditis in Four Dogs," by Laurie B. Cook, Joan R. Coates, Curtis W. Dewey, Sonya Gordon, Matthew W. Miller and Anne Bahr.

Presents information on a study on zonisamide therapy for refractory idiopathic epilepsy in dogs. Findings of the study.

Deals with a study on the retrospective comparison of cervical intervertebral disk disease in nonchondrodystrophic large dogs and small dogs. Percentage of dogs that had resolution of cervical hyperesthesia and were able to ambulate unassisted; Number of dogs that required a second surgery.

Thermal radiofrequency (TRF) of the saphenous nerve (a sensory nerve) combined with pulsed radiofrequency (PRF) of the sciatic nerve (a sensory and motor nerve) might relieve intractable stifle osteoarthritis (OA) pain in dogs. The objective was to determine if saphenous nerve TRF induces Wallerian degeneration and if sciatic nerve PRF induces degeneration or dysfunction. Blinded, controlled, randomized, preclinical study. A group of six intact, female Beagle dogs aged 14–16 months. In each dog, one pelvic limb was assigned randomly to the control group and the other to the treatment group. Dogs were anesthetized and, using ultrasonography, radiofrequency electrodes were positioned adjacent to saphenous and sciatic nerves bilaterally; TRF and PRF were performed only in the treatment limb. Motor nerve conduction velocity (MNCV) was measured in both sciatic nerves 2 weeks later, and the dogs were euthanized. Hematoxylin and eosin-stained sections of saphenous and sciatic nerves were examined using light microscopy. Degeneration and inflammation were scored 0 (none) to 3 (severe). A one-tailed, paired Wilcoxon signed-rank test was used to test for differences in scores and MNCV between control and treatment nerves. Degeneration and inflammation scores were higher in treatment saphenous nerves in 5/6 dogs [83%; 95% confidence interval (CI), 36%, 99%]; however, after Bonferroni correction only degeneration score was higher (p = 0.0313). Degeneration, inflammation or decreased MNCV were not observed in sciatic nerves (each outcome: 0/6 nerves, 0%; 95% CI, 0%, 48%). No dogs experienced postprocedural pain or neurological deficits. The degeneration in TRF-treated saphenous nerves appears sufficient to impair transmission. Sciatic nerve PRF did not cause degeneration with attendant motor deficits, consistent with a proposed neuromodulatory mechanism. A clinical trial is needed to confirm the combined techniques produce analgesia without motor deficits in dogs with stifle OA. [ABSTRACT FROM AUTHOR]

Objective--To determine whether frontal-sinus size is associated with syringohydromyelia. Sample Population--Medical records and magnetic resonance images of 62 small-breed dogs. Procedures--Medical records and magnetic resonance images were reviewed retrospectively for evaluation of frontal-sinus size and syringohydromyelia. A Yates-corrected 2-tailed χ² test was used to determine whether an association existed between absent or miniscule frontal sinuses and syringohydromyelia. The strength of the association was evaluated by means of prevalence and odds ratios. Results--Absent or miniscule air-filled frontal sinuses were detected in 28 of 62 (45%) dogs, and syringohydromyelia was detected in 12 of 62 (19%) dogs. Syringohydromyelia was detected in 10 of 28 dogs with absent or miniscule frontal sinuses (prevalence, 36%; 95% confidence interval, 16% to 55%) and in 2 of 34 dogs with larger frontal sinuses (prevalence, 6%; confidence interval, 0% to 15%). The probability of detecting syringohydromyelia in dogs with absent or miniscule air-filled frontal sinuses was significantly greater than the probability of detecting it in dogs with larger frontal sinuses. The prevalence ratio was 6.1, and the odds ratio was 8.9. Conclusions and Clinical Relevance--An association between frontal-sinus size and syringohydromyelia was identified in small-breed dogs, suggesting that the pathogenesis of syringohydromyelia in some instances may involve abnormal development of the entire or supratentorial part of the cranium, as opposed to being limited to the infratentorial part. [ABSTRACT FROM AUTHOR]