Physiological and clinical vestibular vertigo syndromes are commonly characterized by a combination of phenomena involving perceptual, oculomotor, postural, and vegetative manifestations: vertigo, nystagmus, ataxia, and nausea. Most of the central vestibular syndromes and some of the peripheral vestibular syndromes may have a vascular etiology. Episodic vertigo and oculomotor abnormalities are common early symptoms of reduced vertebrobasilar blood flow due to the steep pressure gradient from the aorta to the terminal pontine arteries. To date, at least eight subgroups of anterior inferior cerebellar artery (AICA) infarction have been identified according to the pattern of neurootological presentations, among which the most common is the combined loss of auditory and vestibular functions. Unilateral ischemic lesions of the pontomesencephalic vestibular pathways, which run along the medial longitudinal fasciculus (MLF), predominantly cause vestibular tone imbalance in the roll plane. Unilateral thalamic infarctions may cause contralateral falling, astasia, or contralateral ocular tilt reaction (OTR).

Stroke is a common disorder of the central nervous system, often with secondary or associated neuromuscular manifestations. Stroke-related neuromuscular manifestations include peripheral neuropathy, myopathy, and dysautonomia. This chapter reviews primary as well as secondary neuromuscular manifestations of stroke. Secondary changes in muscles, connective tissues, and peripheral nerves in limbs rendered paretic or spastic by stroke have been demonstrated with electrophysiological, biomechanical, and histopathological methods. Vasculopathy in neurofibromatosis (NF) is rare but is well characterized in the form of intracranial occlusive arterial disease, cervical arteriovenous fistula, and intracranial aneurysm. Hemiplegic atrophy has long been observed in both human subjects and in experimental subhuman primates after upper motor neuron (UMN) lesions. Cardiac arrhythmias including malignant ventricular tachyarrhythmias and atrioventricular (AV) conduction blocks have been frequently described within the first 24 hours after stroke and can cause sudden death.

Disseminated intravascular coagulation (DIC) is a disorder of clotting caused by a cytokine-induced systemic inflammatory response that results in consumption of platelets, coagulation factors, and tissue factor plasma inhibitors (TFPIs). There is a wide differential diagnosis that includes thrombotic thrombocytopenic purpura (TTP), hemolytic uremic syndrome, systemic lupus erythematosus (SLE), catastrophic antiphospholipid syndrome (APS), and Evans syndrome. A peripheral blood smear in DIC often shows schistocytes, fragmented red blood cells (RBCs) that are formed by fibrin RBC adhesion. DIC is a major cause of stroke in medical intensive care units and is a frequent complication of a terminally ill patient. Replacement therapy with platelets and coagulation factors is given to those patients with severe bleeding. Antithrombin III is the most important of the thrombin inhibitors. It has a beneficial effect in improving coagulation factors and organ function and decreasing mortality in the majority of DIC clinical trials.