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UNASSIGNED: Metastatic brain tumors are a common complication of systemic cancer. They tend to have a chronic onset and are located at the gray-white junction of the cerebral hemispheres, those larger than 9.4 mm in diameter are often accompanied by substantial vasogenic edema. Herein, we report a rare case of calcified metastatic adenocarcinoma with Wallerian degeneration. In addition, we discuss the atypical manifestations of brain metastases.
UNASSIGNED: A 71-year-old man who went through stroke-like onset twice during 8 months with a history of resection of the left pulmonary adenocarcinoma 5 years prior was examined. Diffusion weighted magnetic resonance imaging of the brain showed an enlarged open-ring-shaped hyperintensity on the left periventricular white matter and basal ganglia, with Wallerian degeneration on the left cerebral peduncle. Brain computed tomography revealed nodular calcification of the lesion. The pathology of stereotactic biopsy indicated metastatic adenocarcinoma.
UNASSIGNED: When patients present with acute nervous system symptoms and a previous history of cancer, the possibility of metastases should be considered, even if neuroimaging is atypical.

The type, quantity, and potency of the organophosphorus compound (OPC) taken determine the symptoms of OPC poisoning as well as their severity. The exact etiology for organophosphorus (OP) poisoning delay neuropathy regulating Wallerian degeneration is still unknown.
UNASSIGNED: We report here a rare case of a 25-year-old lady with Wallerian degeneration in the brain found in an MRI in a patient after OPC ingestion. MRI of the brain, in our case, shows Wallerian degeneration of the corona radiata, internal capsule, and midbrain.
UNASSIGNED: Some OPCs can lead to OP-induced delayed neuropathy, a form of delayed neurotoxicity in humans (OPIDN). The distal axonopathy\'s (in OPIDN) morphological pattern resembles Wallerian degeneration, which happens in vitro following nerve damage. Although delayed Wallerian degeneration from organophosphate poisoning often affects the peripheral nervous system, it can also affect the central nervous system. Rehabilitation therapy combined with appropriate nursing care has been demonstrated to improve the disease.
UNASSIGNED: Central nervous system involvement after OP poisoning is rare, and MRI of the brain and spinal cord can document evidence of Wallerian degeneration after OP poisoning.

Peripheral nerve injuries (PNIs) that consist of simple nerve severance often result in severe motor impairment and permanent loss of function. Such patients face significant costs and pose major burdens to healthcare systems. Currently, the most promising surgical technique to achieve the best clinical outcome after such PNIs is immediate primary coaptation of severed nerve ends by microsutures (neurorrhaphy). However, recovery is often poor and delayed for many months due to Wallerian degeneration (WD) and slow (1-2 mm/day) axonal outgrowths from severed proximal axons that may not properly reinnervate denervated afferent/efferent targets that have atrophied. In contrast, recent pre-clinical studies using polyethylene glycol (PEG) to facilitate primary nerve repair have greatly improved the rate and extent of sensory and motor recovery and prevented much WD and muscle atrophy. That is, PEG-fused axons rapidly establish proximal-distal axoplasmic/axolemmal continuity, which do not undergo WD and maintain the structure and function of neuromuscular junction (NMJ). PEG-fused axons rapidly reinnervate denervated NMJs, thereby preventing muscle atrophy associated with monthslong denervation due to slowly regenerating axonal outgrowths. We now describe PEG-mediated fusion repair of a digital nerve in each of two patients presenting with a digital laceration resulting in total loss of sensation. The first patient\'s tactile perception improved markedly at 3 days postoperatively (PO). Two-point discrimination improved from greater than 10 mm at initial presentation to 4 mm at 11-week PO, and the Semmes-Weinstein monofilament score improved from greater than 6.65 to 2.83 mm, a near-normal level. The second patient had severe PO edema and scar development requiring a hand compression glove and scar massage, which began improving at 11-week PO. The sensory function then improved for 4 months PO, with both two-point discrimination and Semmes-Weinstein scores approaching near-normal levels at the final follow-up. These case study data are consistent with data from animal models. All these data suggest that PEG-fusion technologies could produce a paradigm shift from the current clinical practice of waiting days to months to repair ablation PNIs with autografts, anucleated nerve allografts, or conduits in which the patient outcome is solely dependent upon axon regeneration over months or years.

Isolated ocular palsies are often associated with a benign process in the pediatric population but early diagnosis is critical to exclude any serious pathology. In this case, a six-year-old female with no significant past medical history presented with isolated right-eye medial deviation. The patient reported right-eye medial deviation for the past several weeks and associated double vision, but denied any pain with eye movements, other cranial nerve changes, or headaches. This case highlights the key radiologic finding which may ultimately allow for a leading diagnosis and inform further management in cases of isolated ocular nerve palsy.

When temporal bone fractures are associated with facial palsy (FP) evolution the medical team have no much time to make a decision: to do or not to do a surgical approach? How to evaluate the necessity? When to do it and when is the correct time?

暂无摘要。

Wallerian degeneration is defined as axonal fiber and myelin sheath degeneration that affects myelinated axons within the peripheral or central nervous system. Wallerian degeneration or anterograde axonal degeneration before myelination is rarely reported. Involvement of both corticospinal tracts (CSTs) is rarely documented in the literature. We present the postmortem neuropathologic findings of a 1-week-old male neonate born at 23 weeks of gestation with bilateral CST degeneration extending from the posterior limb of the internal capsule through the brainstem into the lumbar spinal cord. Abundant CD68- and CD163-positive macrophages were the prominent histopathology in both CSTs. The cerebrum, brainstem, and spinal cord were unmyelinated, as expected. In contrast, the spinal nerve roots demonstrated early myelination. This case illustrates that Wallerian degeneration occurs in unmyelinated axis cylinders.

暂无摘要。

The corticobasal syndrome (CBS) is heterogeneous in terms of postmortem neuropathology. While it has been previously studied with antemortem neuroimaging, clinicopathologic features of corticobasal syndrome associated with cerebrovascular pathology (vascular CBS) have yet to be reported.
To identify vascular CBS, we searched the database of the CurePSP Brain Bank for patients with a clinical diagnosis of CBS who failed to meet neuropathologic criteria for corticobasal degeneration (CBD) or other neurodegenerative disease processes, but who had significant cerebrovascular pathology. Hemibrains were assessed macroscopically and processed for histological assessment. Medical records were reviewed to characterize clinical features of vascular CBS.
Of 217 patients with an antemortem diagnosis of CBS, we identified three patients with vascular CBS. Multiple infarcts in the watershed regions (frontal lobe and motor cortex), periventricular white matter, thalamus, and basal ganglia were observed in two patients. One patient had no cortical infarcts, but had multiple white matter infarcts and corticospinal tract degeneration. All were clinically thought to have CBS based on progressive asymmetric motor symptoms, including rigidity and apraxia, as well as cognitive impairment. Antemortem imaging studies showed findings of chronic cerebrovascular disease, with infarcts or white matter pathology.
This autopsy study of vascular CBS shows that, while rare, cerebrovascular pathology involving the frontal lobe, white matter tracts, basal ganglia, thalamus, and corticospinal tract can underlie clinical features suggestive of CBS. When neuroimaging suggests an alternative explanation, including chronic infarcts in critical regions, caution is merited in considering CBD as the underlying pathology.