Hemorrhage into the basis pontis frequently extends rostrally into the midbrain and appears to produce coma by interference with midbrain reticular function. This condition is associated with pinpoint pupils, presumably reflecting both parasympathetic irritation as well as sympathetic outflow disruption. Importantly, however, most patients presenting in coma with pinpoint pupils are suffering from an opiate overdose and not specific pontine dysfunction. Naloxone quickly reverses opiate pupillary changes but has no effect on pontine lesions. Patients with pontine lesions that cause coma from involvement of midbrain reticular dysfunction may also have a flaccid hemiparesis or paraparesis, irregular respirations termed apneustic, and a variety of extraocular palsies. These problems may include conjugate deviation of the eyes toward the hemiparetic body if the PPRF has a lesion, unilateral or bilateral sixth nerve palsies or an internuclear ophthalmoplegia if the MLF has a lesion. Cold caloric testing usually clarifies the ocular dysfunction.
Primary pontine lesions without midbrain involvement may mimic coma as the "locked-in" syndrome by interrupting almost all efferent pathways from the cerebral cortex. Infarction of the basis pontis disrupts the corticospinal tracts (producing tetraplegia), the PPRF and abducens nuclei (eliminating conjugate horizontal eye movements), and the facial nerves in their course around the abducens nuclei (resulting in complete facial paralysis). Because the MRF is spared, however, the patient is awake and alert; and because the sensory pathways have migrated to a posterior position in the pons, both the auditory and somatosensory systems are functional. The only voluntary motor act of which the patient is capable is conjugate vertical eye movements. When the patient is not actively moving the eyes, spontaneous vertical movements known as ocular bobbing may develop.
Although this condition was previously emphasized because of the possibility that a sentient patient would mistakenly be judged comatose, the advent of thrombolytic therapy for cerebrovascular diseases mandates that these patients be identified rapidly so that they may be considered for intravenous recombinant tissue plasminogen activator (rt-PA) treatment. At present, studies of intra-arterial thrombolysis are in progress.
The locked-in state is occasionally mimicked by severe neuropathic disorders (e.g., acute inflammatory polyneuropathy, the Guillain-Barre(c) syndrome) and other widespread peripheral disorders.
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