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Peripheral neuropathy (PN) is a common neurological problem defined as a dysfunction of sensory, motor, and autonomic nerves. The presence of peripheral neuropathy has recently been noticed in Parkinson's disease (PD) This comorbidity is concerning as it increases the burden on patients whose motor functions are previously compromised. A comprehensive computer-based literature review utilizing multiple peer-reviewed databases (e.g., Embase, PsycINFO, CINAHL, etc.) was conducted. There is evidence for the utility of robust diagnostic criteria to distinguish between large fiber neuropathy (LFN) and small fiber neuropathy (SFN). Some studies have established links between prolonged L-DOPA exposure and prevalence with increased levels of homocysteine (HCY) and methylmalonic acid (MMA) as pathological underlying mechanisms. PN in PD patients with relatively truncated exposure to L-DOPA therapy may have underlying mutations in the Parkin and MHTFR gene or separate mitochondrial disorders. Vitamin B12 and cobalamin deficiencies have also been implicated as drivers of PN. Accumulation of phosphorylated α-synuclein is another central feature in PN and deems urgent exploration via large cohort studies. Importantly, these underlying mechanisms have been linked to peripheral denervation. This review delves into the potential treatments for PN targeting B12 deficiencies and the use of COMT inhibitors along with other novel approaches. Avenues of research with powerful randomized controlled and long-term cohort studies exploring genetic mechanisms and novel treatment pathways is urgently required to alleviate the burden of disease exerted by PN on PD.

Delayed enlargement of a traumatic cerebral contusion can occur subsequent to an initial CT scan, and this can lead to neurological deterioration, brain herniation, and death. Herein, we describe the case of a 76-year-old male who experienced an intracerebral hemorrhage subsequent to a fall and whose injury worsened over time. We summarize the current recommendations in the literature for when to initiate follow-up imaging in patients with traumatic head injury, the risk factors for progression, and the role of close clinical monitoring and serial imaging in managing such patients. Finally, we illustrate how these recommendations were applied in our case.

Cryptococcal Meningitis (CM) is caused by members of the yeast species, Cryptococcus neoformans. Although C.neoformans can cause infection in any part of the body, the fungus prefers to invade regions of the lungs and CNS [1]. The infection is thought to be acquired through the respiratory tract, and reaches the meninges through the blood circulation [1]. Symptoms of CM include headaches, malaise, fever, and changing psycho-mental stability. CM is most commonly recognized as an opportunistic infection in immunocompromised individuals, especially those suffering from HIV/AIDS, liver cirrhosis or sarcoidosis [2]. Hence, CM risk is usually overlooked or totally ignored during the differential diagnosis of immunocompetent individuals who present meningitis like symptoms. Recent reports have indicated rising prevalence of CM in individuals who are believed to be immunocompetent, resulting in delayed or misdiagnosis of such patients [3]. Other factors are emerging to be important determinants when diagnosing a patient with meningitis like symptoms. Such factors include environmental factors originally believed to be important in Africa or in tropical environments. Environmental factors (as they relate to CM) can be defined as any factor originating from the environment that results in immunodeficiency, either by a significant decrease in white blood cells count or by interfering with normal immunological response of the body.