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1. Pingree GM, Fleming C, Reavey-Cantwell J, et al. Neurosurgical causes of pulsatile tinnitus: contemporary update. Neurosurgery 2022;90:16 1–69

This review details the most common treatable neurosurgical entities that can present with pulse-synchronous tinnitus: Cervical carotid stenosis, ICA dissection, FMD, Petrous carotid dissection/aneurysm, Cavernous carotid dissection/aneurysm, AVM/AVFs, glomus tumors, and various venous stenoses, and thrombosis, among others.

Patients with internal carotid artery dissection can present unilateral headaches, posterior cervical pain, cranial nerve palsies, oculosympathetic palsy, and cerebral or retinal ischemia. Objective bruits may be detected on arterial auscultation. Pulsatile tinnitus has been reported in 5% to 15% of patients with ICAD but is infrequently the sole presenting symptom. ICADs are typically identified on MRI/ magnetic resonance angiography (MRA) or computed tomography (CT) angiography, or conventional angiography.  Many cases of ICAD are self-limiting, with stenosis resolving in approximately 46% to 90% of patients over a 3- to 6-mo interval. Invasive options such as angioplasty and stenting are reserved for cases of hemodynamically significant stenosis or expanding lesions with progressive stenosis. In the majority of cases of PT secondary to ICAD, PT spontaneously improves together with the arterial injury over the course of 2 to 6 months.

Patients with petrous carotid dissection may present with deafness, vertigo, and facial nerve weakness and even nausea, vomiting, and cranial nerve involvement with more severe diseases. PT can be the sole presenting symptom. As in the cervical carotid, treatment of spontaneous and asymptomatic dissections is typically medical management with antiplatelet medications. Endovascular treatment can be given for patients with increasing pseudoaneurysm size or recurrent ischemia, despite medical management.  Improvement in PT symptoms has been reported after both medical treatment and endovascular treatment of petrous segment dissections.

2 tables, 6 figures with MR, CT and catheter angio

2. Delev D, Hakvoort K, Krüger MT, et al. Choroidal artery ischemic events after temporal lobe epilepsy surgery: clinical outcome, quality of life, and surgical pitfalls. J Neurosurg 2022;136:53 6–42. Available from: https://thejns.org/view/journals/j-neurosurg/aop/article-10.3171-2021.1.JNS203092/article-10.3171-2021.1.JNS203092.xml

In epilepsy surgery, severe motor deficits as a postoperative complication are rare, but can lead to devastating postoperative conditions, reducing a patient’s HRQoL and life independency. In most cases, the pathophysiological cause of such severe neurological deficits is vascular events leading to ischemic lesions, predominantly in the territory of either the choroidal arteries—the anterior choroidal artery (AChA) and posterior choroidal artery (PChA)—or small perforating arteries. The AChA supplies crucial regions of the posterior limb of the internal capsule, the lateral geniculate body, and the optic tract, as well as the medial area of the pallidum. The AChA consists of a cisternal segment that runs through the choroidal fissure and a plexus part that supplies the choroidal plexus, with its entry point defined as the choroidal point. The PChA and small perforating arteries supply the basal ganglia, thalamus, and parts of the dorsal brainstem. The clinical triad of AChA infarctions consists of hemiparesis, hemihypesthesia, and visual field deficits. In rare cases, when the dominant hemisphere is involved, aphasia can also occur.

The aim of this study was to evaluate the rate of ischemic events after standard surgical procedures for drug resistant TLE, such as anterior temporal lobectomy and selective amygdalohippocampectomy, and report their clinical course. Four hundred twenty-two consecutive patients undergoing temporal resections for drug-resistant TLE were retrospectively analyzed. The overall complication rate was 7.8% (n = 33). Fourteen patients (3.3%) suffered from ischemic events causing 6 permanent motor deficits, 3 with permanent aphasias, and 6 visual field defects that exceeded quadrantanopia. In 8 patients with anterior choroidal artery infarction, accounting for 57% of all ischemic events, infarction volume correlated positively with the occurrence of new permanent neurological deficits. Choroidal artery infarctions are rare but relevant complications after TLE surgery, presenting with variable clinical courses ranging from devastating neurological deterioration to complete recovery. Despite the occurrence of postoperative infarction, most patients report improvement of HRQoL after TLE surgery.

3 figures, 2 tables with MR and schematic drawing of possible pitfall during resection due to aberrant AChA course

3. Vemuri P, Decarli C, Duering M. Imaging markers of vascular brain health: quantification, clinical implications, and future directions. Stroke 2022;53:41 6–26. Available from: https://www.ahajournals.org/doi/10.1161/STROKEAHA.120.032611

The authors largely focus on the aspect of small vessel disease because it contributes to about 50% of dementias worldwide and do not expand on acute stroke–related changes. With this approach, they have 3 goals in mind. First, they present key imaging markers for measuring CVD starting with traditional lesion markers followed by methods available for measuring early CVD-related brain injury. Then they discuss clinical implications and relevance of these CVD imaging markers for cognitive decline, incident dementia, and disease progression in Alzheimer disease (AD) and Alzheimer related dementias. Finally, they present their perspective on the outlook of research in this area.

Increasing WMH burden seen on T2 weighted or fluid-attenuated inversion recovery MRI is a common consequence of the aging process, exacerbated by vascular risk factors, particularly hypertension, and generally increases over time as individuals age. This process, however, may evolve over decades as recent studies indicate white matter injury associated with emerging WMH can begin during middle life. Numerous observations support the clinical relevance of WMH. Not only is WMH burden associated with cognitive impairment in cross-sectional studies, but evolution of WMH are associated with declines in both memory and executive function. Furthermore, extensive WMH predicts incident MCI, stroke, and dementia.

Microbleeds or microhemorrhages are microscopic (≈200 μm) areas of blood leakage from injured vessels. Following the leakage of blood from a damaged vessel, hemosiderin is deposited in macrophages and these deposits are visible as hypointense lesions <10 mm in size on T2* GRE and SWI. SWI offers greater reliability and sensitivity in detecting microbleeds in comparison to T2* GRE. Microbleeds can occur in either subcortical or lobar cortical brain regions. Subcortical microbleeds are associated with small vessel disease pathologies and vascular risk factors, whereas lobar cortical microbleeds are associated mostly with CAA where amyloid deposits in the vessel wall lead to injury and subsequent blood leakage. Focal tracer uptake in the areas of cerebral microbleeds as seen on amyloid positron emission tomography supports the causal relationship between amyloid and microbleeds. The presence of microbleeds is clinically relevant as meta-analyses consistently show associations with cognitive dysfunction.

With the emergence of increased imaging resolution of 7 Tesla ultrahigh field MRI, small cortical lesions (small cavitations) termed as cortical microinfarcts can now be detected, although most microinfarcts detected on histopathologic examination are even smaller and escape high-resolution scans.  Cortical microinfarcts have an independent effect on cognitive impairment and dementia after accounting for traditional CVD markers such as WMH, microbleeds, and infarctions.

2 figures with MR

4. Ganapathy A, Diaz EJ, Coleman JT, et al. Tumor syndromes: neurosurgical evaluation and management. Neurosurg Clin N Am 2022;33:91 –104. Available from: https://doi.org/10.1016/j.nec.2021.09.007

Li-Fraumeni syndrome (LFS) is caused by a mutation in the TP53 gene located on chromosome 17p13. P53 is a tumor suppressor tetrameric protein that acts as a gatekeeper in regulation of cell cycle arrest, apoptosis, senescence, and DNA repair. The prevalence of this disorder is one in 5000, and these individuals have a life-long risk of multiple tumors in various organ systems.  Germline TP53 mutations are found in 50%of pediatric adrenocortical tumors, 2% to 10% of childhood brain tumors, 9% of rhabdomyosarcoma, and 2% to 3% of osteosarcomas. Approximately half of patients with Li-Fraumeni syndrome will develop a cancer by age 30. Some common brain tumors in patients with LFS include choroid plexus carcinoma (CPC), MB, astrocytoma, and, with less frequency, ependymoma.

Gorlin syndrome (GS), also known as nevoid basal cell carcinoma syndrome or Gorlin-Goltz syndrome, is a rare AD cancer syndrome inherited with high penetrance but variable expression. The prevalence varies between 1/31,000 and 1/ 235,800, with no predilection between men and women. The disorder is characte