Hashimoto's encephalopathy (HE), also known as steroid-responsive encephalopathy, is associated with autoimmune-mediated thyroiditis. Onset is typically gradual often with evolution over the course of months. Characteristic symptoms include impaired concentration and memory, delusions, hallucinations, personality changes, incoordination, tremor, hemiparesis, seizures, and speech difficulties. Diagnosis is predicated upon discovery of elevated anti-thyroid antibodies, specifically anti-thyroid peroxidase (TPO) or anti-M antibodies. Some patients may also present with subclinical hypothyroidism but many are euthyroid. Of note, neither thyroid function tests or antibody titers correlate with disease severity. Other common laboratory findings include elevations in sedimentation rate, liver enzymes, and cerebrospinal fluid (CSF) protein. Radiological work-up, including cerebral angiography, is often normal. Successful treatment includes administration of steroids and/or intravenous immunoglobulin (IVIg) or plasmapheresis. We describe a case of a 74-year-old male who presented for evaluation of abrupt onset confusion ultimately determined to be a consequence of autoimmune-mediated thyroiditis.

Copper deficiency is a rare and potentially treatable cause of myeloneuropathy. The most common causes of acquired copper deficiency include malabsorption following gastric surgery and excessive zinc supplementation. Clinical manifestations can be localized to the dorsal spinal cord and present similarly to those that characterize classic vitamin B12 deficiency. In this report, we present the case of a 76-year-old female with copper deficiency myeloneuropathy as a presumed consequence of advanced systemic sclerosis (SSc).

Studies exploring the association between pesticide exposure and Parkinson's disease (PD) are largely limited to rural populations with occupational exposure. We could find no literature regarding PD occurring after ingestion of a pesticide. We present a case from our clinic of a man who developed PD following ingestion of a liquid pesticide during a suicide attempt. PD was diagnosed, and the patient's symptoms improved following initiation of carbidopa/levodopa. This case illustrates the potential role of ingested pesticide exposure in provoking and accelerating the manifestations of PD.

Systemic lupus erythematosus (SLE) is known for marked heterogeneity of clinical manifestations and pathogenesis with the potential of affecting virtually every organ system. Neuropsychiatric manifestations of systemic lupus erythematosus are difficult to recognize and treat as they remain one of the least understood complications of this disease. Our case describes a 42-year-old female who presented to the emergency department with proximal weakness of the left lower extremity, magnetic resonance imaging (MRI) of the brain revealed a small infarct in the medial left temporal lobe. Workup was remarkable for elevated inflammatory markers. The patient was discharged on appropriate medical therapy however returned to the emergency department one month later after a witnessed focal seizure. Neuroimaging was consistent with cerebral vasculitis and autoimmune workup revealed a diagnosis of SLE. Our case highlights the importance of recognizing that neuropsychiatric manifestations of SLE often occur in absence of other systemic manifestations and can be the initial presentation of SLE. Maintaining a high clinical suspicion for Neuropsychiatric Systemic Lupus Erythematosus (NPSLE) could afford the ability to halt disease progression in the earliest of phases and thus improve quality of life through early administration of appropriate pharmacotherapy.

While the clinical presentation of systemic sarcoidosis is well established, identification of isolated neurologic sarcoidosis remains a diagnostic challenge. Isolated neurologic sarcoidosis, or neurosarcoidosis, presents in a manner that is often indistinguishable from other neurological diseases. Common clinical features include headache, encephalopathy, gait disturbance, seizure, behavioral abnormalities, sleep difficulties, loss of appetite, cranial mononeuropathy (including visual, auditory, and vestibular dysfunction), myelopathy, radiculopathy, myopathy, and peripheral neuropathy. While probable diagnosis requires only evidence of inflammation on cerebrospinal fluid studies or magnetic resonance imaging, tissue biopsy with pathologic findings of noncaseating granulomas is required for definitive diagnosis. We present the case of a 54-year-old male with headache, episodic confusion, and gait disturbance attributed to probable neurologic sarcoidosis.