Abstract Snake and spider bites, as well as scorpion sting envenoming, are neglected diseases affecting millions of people all over the world. Neurological complications vary according to the offending animal, and are often directly related to toxic effects of the venom, affecting the central nervous system, the neuromuscular transmission, the cardiovascular system, or the coagulation cascade. Snake bite envenoming may result in stroke or muscle paralysis. Metalloproteinases and other substances (common in vipers and colubrids) have anticoagulant or procoagulant activity, and may induce ischemic or hemorrhagic strokes. The venom of elapids is rich in neurotoxins affecting the neuromuscular transmission at either presynaptic or postsynaptic levels. The clinical picture of scorpion sting envenoming is dominated by muscle weakness associated with arterial hypertension, cardiac arrythmias, myocarditis, or pulmonary edema. These manifestations occur as the result of release of catecholamines into the bloodstream or due to direct cardiac toxicity of the venom. Cerebrovascular complications have been reported after the sting of the Indian red scorpion. Intracranial hemorrhages occur in the setting of acute increases in arterial blood pressure related to sympathetic overstimulation, and cerebral infarctions are related to either cerebral hypoperfusion, consumption coagulopathy, vasculitis, or cardiogenic brain embolism. Three main syndromes result from spider bite envenoming: latrodectism, loxoscelism, and funnel-web spider envenoming. Latrodectism is related to neurotoxins present in the venom of widow spiders. Most cases present with headache, lethargy, irritability, myalgia, tremor, fasciculation, or ataxia. Loxoscelism is caused by envenoming by spiders of the family Sicariidae. It may present with a stroke due to a severe coagulopathy. The venom of funnel-web spiders also has neurotoxins that stimulate neurotransmitter release, resulting in sensory disturbances and muscle paralysis. Proper management of the envenomed patient, including prompt transport to the hospital, correction of the hemostatic disorder, ventilatory support, and administration of antivenom, significantly reduce the risk of neurological complications which, in turn, reduce the mortality and improve the functional outcome of survivors.