Alzheimer’s disease (AD) is the leading cause of dementia worldwide. The disease is characterized by the abnormal accumulation of amyloid β (Aβ) protein creating neuritic plaques, hyperphosphorylated tau (p-tau) protein forming intracellular tangles, and neuronal degeneration. Pathological changes related to abnormal Aβ and p-tau accumulation may begin more than fifteen years before the clinical diagnosis of AD is made. The glymphatic system is the brain’s waste clearance pathway that prevents the accumulation of these abnormal proteins and macromolecules. Glymphatic clearance is negatively affected by physiological conditions such as sleep deprivation, and pathological conditions such as traumatic brain injury and hemorrhagic strokes. These physiological and pathological conditions are strong risk factors for AD. In conclusion, impaired glymphatic clearance is an important pathogenetic mechanism for AD.

Cerebral amyloid angiopathy (CAA) is a common cause of lobar intracerebral hemorrhage in the elderly. It is also associated pathologically with Alzheimer’s disease (AD). Both CAA and AD share similar pathology of deposition amyloid beta fibrils (Aβ). Aβ is deposited mainly in the neurites in AD and vascular walls in CAA. Aβ is formed inside the brain parenchyma from the amyloid precursor protein. It is easier to understand how Aβ is deposited in the cerebral neurites in AD. However, the pathogenesis of CAA is still largely unknown. It is difficult to understand or visualize how Aβ fibrils formed inside the brain can be deposited against the cerebral perfusion pressure to be deposited in the cerebral and meningeal arterial walls. We encountered an unusual clinical case of acute aneurysmal subarachnoid hemorrhage which was followed after a few years with localized CAA involving mainly the sites of the subarachnoid hemorrhage. We reviewed the formation of Aβ and postulated how the Aβ fibrils are transported retrogradely toward the cerebral arteries and deposited in the arterial walls resulting in the final pathology of CAA. There is a clear disturbance of the glymphatic system, the aquaporin-4 channel, and the parenchymal border macrophages.

Idiopathic intracranial hypertension (IIH) is defined as raised intracranial pressure of unknown etiology. Looking for underlying causes needs to be undertaken before the diagnosis is confirmed and managed accordingly. We are reporting a rare and unique case of a patient with the clinical diagnosis of idiopathic intracranial hypertension or pseudotumor cerebri. She is not obese and not taking any predisposing medication. Her first magnetic resonance imaging (MRI) and magnetic resonance venogram (MRV) were reported as showing left transverse sinus thrombosis. She was treated with anticoagulation. Her final diagnosis of left transverse sinus compression by a meningioma en plaque (MEP) was finally made with a repeat MRI. A high index of suspicion of unusual causes is important when IIH presents in an atypical patient or with an atypical presentation. The prognosis and management of real IIH and raised intracranial pressure due to other causes are different.

This case describes a 30-year-old Hispanic male who presented with a significant headache that started after a period of weightlifting and squatting. The patient was diagnosed with a basilar artery dissection. His only complaint was a headache that was exacerbated with exertion and sexual activity; there were no neurologic deficits. The diagnosis of basilar artery dissection was established and supported by findings on the CT angiogram of his head and neck. Basilar artery dissections are rarely seen, as they are likely underrecognized due to their varying clinical presentations; however, it is important to consider these phenomena due to the risk of progression and high morbidity rates.

Wernicke’s encephalopathy (WE) is a neuropsychiatric condition caused by thiamine deficiency often associated with alcoholism. Other less common causes include prolonged gastroenterology problems or dietary insufficiencies associated with hyperemesis gravidarum, bariatric surgery, and eating disorders. Prolonged WE without proper treatment can lead to the chronic and irreversible condition, Wernicke-Korsakoff syndrome. Despite being known for its classic triad of clinical symptoms (nystagmus/ophthalmoplegia, gait ataxia, and confusion), WE patients more commonly present with non-specific symptoms of altered mental status. Obscure clinical presentations often led to delays in the appropriate of patients with WE. We are presenting a case of WE that is unusual because the underlying cause is schizophrenia and the lack of alcohol use. For a punctual diagnosis, a high index of suspicion is essential to prevent further exacerbation of neuronal death seen in WE. IV thiamine should be administered to any patient with acute encephalopathy or altered mental status, given its low cost and lack of side effects.

Isolated hypoglossal nerve (CN XII) palsy is rare. Neurological complications of multiple myeloma (MM) are quite common, most often due to hyperviscosity and paraprotein-related neuropathy. Direct compression of CN XII can be caused by plasmacytoma, yet direct invasion by MM is extremely rare. We are reporting a very unusual case of a 45-year-old man who presented with an isolated right CN XII palsy. The cause revealed by MRI is stenosis of the hypoglossal canal resulting from lytic bony erosion. Despite negative serum and urine protein electrophoresis tests, the final diagnosis of oligosecretory MM was confirmed by serum-free light chain test and bone marrow biopsy. The causes and diagnosis of isolated XII nerve palsy and oligosecretory MM are discussed.