Al-Zahrawi (936-1013 AD): On the Surgical Treatment of Neurological Disorders by the Father of Operative Surgery.

BACKGROUND: Medical knowledge during the medieval ages flourished under the influence of great scholars of the Islamic Golden age such as Ibn Sina (Latinized as Avicenna), Abu Bakr al-Razi (Rhazes), and Abu al-Qasim Khalaf ibn al-Abbas al-Zahrawi, known as Albucasis. Much has been written on al-Zahrawi's innovation in various disciplines of medicine and surgery. In this article, we focus for on the contributions of al-Zahrawi toward the treatment of neurological disorders in the surgical chapters of his medical encyclopedia, Kitab al-Tasrif (The Method of Medicine). METHODS: Excerpts from a modern copy of volume 30 of al-Zahrawi's Kitab al-Tasrif were reviewed and translated by the primary author from Arabic to English, to further provide specific details regarding his neurosurgical knowledge. In addition, a literature search was performed using PubMed and Google Scholar to review prior reports on al-Zahrawi's neurosurgical instructions. RESULTS: In addition to what is described in the literature of al-Zahrawi's teachings in cranial and spine surgery, we provide insight into his diagnosis and management of cranial and spinal trauma, the devices he used, and prognostication of various traumatic injuries. CONCLUSIONS: Al-Zahrawi was a renowned physician during the Islamic Golden age who made significant contributions to the diagnosis and treatment of neurological conditions, particularly cranial and spinal cord injuries. He developed innovative surgical techniques for trephination and spinal traction, which are still used in modern neurosurgery. His insights make him worthy of recognition as an important figure in the history of neurological surgery.

Seizure and anatomical outcomes of repeat laser amygdalohippocampotomy for temporal lobe epilepsy: A single-institution case series.

OBJECTIVE: In patients with treatment-refractory temporal lobe epilepsy (TLE), a single stereotactic laser interstitial thermotherapy (LITT) procedure is sometimes insufficient to ablate epileptogenic tissue, particularly the medial structures often implicated in TLE. In patients with seizure recurrence after initial ablation, the extent to which a second ablation may achieve improved seizure outcomes is uncertain. The objective of this study was to investigate the feasibility and potential efficacy of repeat LITT amygdalohippocampotomy as a worthwhile strategy for intractable temporal lobe epilepsy by quantifying changes to targeted mesial temporal lobe structures and seizure outcomes. METHODS: Patients who underwent two LITT procedures for drug-resistant mesial TLE at our institution were included in the study. Lesion volumes for both procedures were calculated by comparing post-ablation intraoperative sequences to preoperative anatomy. Clinical outcomes after the initial procedure and repeat procedure were classified according to Engel scores. RESULTS: Five consecutive patients were included in this retrospective case series: 3 with right- and 2 with left-sided TLE. The median interval between LITT procedures was 294 days (range: 227-1918). After the first LITT, 3 patients experienced class III outcomes, 1 experienced a class IV, and 1 experienced a class IB outcome. All patients achieved increased seizure freedom after a second procedure, with class I outcomes (3 IA, 2 IB). CONCLUSIONS: Repeat LITT may be sufficient to achieve satisfactory seizure outcomes in some individuals who might otherwise be considered for more aggressive resection or palliative neuromodulation. A larger study to establish the potential value of repeat LITT amygdalohippocampotomy vs. other re-operation strategies for persistent, intractable temporal lobe epilepsy is worth pursuing.

Thalamic neuromodulation in epilepsy: A primer for emerging circuit-based therapies.

INTRODUCTION: Epilepsy is a common, often debilitating disease of hyperexcitable neural networks. While medically intractable cases may benefit from surgery, there may be no single, well-localized focus for resection or ablation. In such cases, approaching the disease from a network-based perspective may be beneficial. AREAS COVERED: Herein, the authors provide a narrative review of normal thalamic anatomy and physiology and propose general strategies for preventing and/or aborting seizures by modulating this structure. Additionally, they make specific recommendations for targeting the thalamus within different contexts, motivated by a more detailed discussion of its distinct nuclei and their respective connectivity. By describing important principles governing thalamic function and its involvement in seizure networks, the authors aim to provide a primer for those now entering this fast-growing field of thalamic neuromodulation for epilepsy. EXPERT OPINION: The thalamus is critically involved with the function of many cortical and subcortical areas, suggesting it may serve as a compelling node for preventing or aborting seizures, and so it has increasingly been targeted for the surgical treatment of epilepsy. As various thalamic neuromodulation strategies for seizure control are developed, there is a need to ground such interventions in a mechanistic, circuit-based framework.

Prostatic abscess: a rare complication of staghorn calculi.

A staghorn calculus is a calculus accommodating the majority of a renal calyx extending into the renal pelvis. A conservative approach to its treatment may lead to high morbidity and mortality rates. Such morbidity usually manifests with renal failure, obstructed upper urinary tractand/or life-threatening sepsis. Prostatic abscesses have never been associated with staghorn calculi in the literature. We report a case of a 70-year-old man who presented with sepsis, which was found to originate from a complex prostatic abscess. The patient had no history of urinary tract infections or risk factors. The authors believe that the incidentally identified staghorn calculi promoted the growth of Proteus mirabilis which led to the development of the prostatic abscess. The patient underwent a transurethral resection and drainage of the abscess following a failed course of antibiotic therapy. This case also highlights the paucity of guidelines available in treating prostatic abscesses.

Direct Intracranial Injection of AAVrh8 Encoding Monkey ß-N-Acetylhexosaminidase Causes Neurotoxicity in the Primate Brain.

GM2 gangliosidoses, including Tay-Sachs disease and Sandhoff disease, are lysosomal storage disorders caused by deficiencies in ß-N-acetylhexosaminidase (Hex). Patients are afflicted primarily with progressive central nervous system (CNS) dysfunction. Studies in mice, cats, and sheep have indicated safety and widespread distribution of Hex in the CNS after intracranial vector infusion of AAVrh8 vectors encoding species-specific Hex α- or ß-subunits at a 1:1 ratio. Here, a safety study was conducted in cynomolgus macaques (cm), modeling previous animal studies, with bilateral infusion in the thalamus as well as in left lateral ventricle of AAVrh8 vectors encoding cm Hex α- and ß-subunits. Three doses (3.2 × 1012 vg [n = 3]; 3.2 × 1011 vg [n = 2]; or 1.1 × 1011 vg [n = 2]) were tested, with controls infused with vehicle (n = 1) or transgene empty AAVrh8 vector at the highest dose (n = 2). Most monkeys receiving AAVrh8-cmHexα/ß developed dyskinesias, ataxia, and loss of dexterity, with higher dose animals eventually becoming apathetic. Time to onset of symptoms was dose dependent, with the highest-dose cohort producing symptoms within a month of infusion. One monkey in the lowest-dose cohort was behaviorally asymptomatic but had magnetic resonance imaging abnormalities in the thalami. Histopathology was similar in all monkeys injected with AAVrh8-cmHexα/ß, showing severe white and gray matter necrosis along the injection track, reactive vasculature, and the presence of neurons with granular eosinophilic material. Lesions were minimal to absent in both control cohorts. Despite cellular loss, a dramatic increase in Hex activity was measured in the thalamus, and none of the animals presented with antibody titers against Hex. The high overexpression of Hex protein is likely to blame for this negative outcome, and this study demonstrates the variations in safety profiles of AAVrh8-Hexα/ß intracranial injection among different species, despite encoding for self-proteins.