Anti-glutamic acid decarboxylase (GAD) antibodies have been discovered in a variety of neurological syndromes with unique presentations. These syndromes include limbic encephalitis (LE), stiff person syndrome (SPS), opsoclonus-myoclonus-ataxia syndrome, cerebellar ataxia, status epilepticus, and palatal myoclonus among others. We present two patients who presented with Guillain-Barré (GBS) and myasthenia gravis (MG) like syndromes, who were found to have anti-GAD antibodies. These case reports highlight the complex presentation of patients with neurological disorders associated with anti-GAD antibodies. The proper identification of anti-GAD antibody’s presence has proven to be beneficial in treatment and provide enhanced quality of life.

Aneurysmal subarachnoid hemorrhage is a life-threatening event that can cause permanent disability. This life-threatening event can be further complicated by subsequent cardiac and pulmonary disability. The presence of a neurogenic cardiomyopathy and pulmonary edema increases the morbidity and mortality of patients who suffer from aneurysmal subarachnoid hemorrhage. In this paper, we discuss a 39-year-old woman who presented to the emergency department (ED) with a chief complaint of a pounding headache with associated nausea and vomiting for the past three days. She had a past medical history significant only for migraines. During her stay in the ED, she began to exhibit signs of altered consciousness, hemoptysis, and respiratory compromise. Neuroimaging showed evidence of subarachnoid hemorrhage. The exact source of her subarachnoid hemorrhage could not be located with neuroimaging or angiography. Her clinical course was complicated by pulmonary edema and neurogenic stunned myocardium, and is still ongoing.

Cortical superficial siderosis (cSS), also referred to as sulcal siderosis, is a neurological condition characterized by hemosiderin subpial deposits in the cortical sulci over the convexities of cerebral hemispheres. These deposits are further found sparingly in the spinal cord, brainstem, and cerebellum. Patients typically present with transient focal neurological symptoms that make cSS challenging to differentiate from other acute neurological processes such as transient ischemic attacks (TIA), focal seizures, and acute convexity subarachnoid hemorrhage (cSAH). This condition is presently recognized as a characteristic feature of the age-associated disorder referred to as cerebral amyloid angiopathy (CAA). This paper describes a patient who presented with transient neurologic symptoms, first suspected to be secondary to acute subarachnoid hemorrhage (SAH), found to have cSS and cerebral amyloid angiopathy.

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