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CARDINAL MANIFESTATIONS OF NEUROLOGIC DISEASE
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reviewed by Berger and colleagues It is interesting, however, that patients with high spinal transections and inability to breathe can still sense changes in lung volume, attesting to a nonspinal afferent route to the brainstem from lung receptors, probably through the vagus nerves In addition, there are receptors located between pulmonary epithelial cells that respond to irritants such as histamine and smoke They have been implicated in the genesis of asthma Also there are J-type receptors that are activated by substances in the interstitial uid of the lungs These are capable of inducing hyperpnea and probably play a role in driving ventilation under conditions of pulmonary edema Both the diaphragm and the accessory muscles of respiration contain conventional spindle receptors, but their role is not clear; all that can be said is that the diaphragm has a paucity of these receptors compared with other skeletal muscles (a property shared with extraocular muscles) and is therefore not subject to spasticity with corticospinal lesions or to the loss of tone in states such as REM sleep, in which gamma motor neuron activity is greatly diminished Dyspnea The common respiratory sensations of breathlessness, air hunger, chest tightness, or shortness of breath, all subsumed under the term dyspnea, have de ed neurophysiologic interpretation In animals, Chen and colleagues from Eldridge s laboratory have demonstrated that neurons in the thalamus and central midbrain tegmentum re in a graduated manner as respiratory drive is increased These neurons are in uenced greatly by afferent information from the chest wall, lung, and chemoreceptors and are postulated to be the thalamic representation of sensation from the thorax that is perceived at a cortical level as dyspnea However, functional imaging studies indicate that various areas of the cerebrum are activated by dyspnea, mainly the insula and limbic regions Aberrant Respiratory Patterns Many of the most interesting respiratory patterns observed in neurologic disease are found in comatose patients, and several of these patterns have been assigned localizing value, some of uncertain validity: central neurogenic hyperventilation, apneusis, and ataxic breathing These are discussed in relation to the clinical signs of coma (Chap 17) and sleep apnea (Chap 19) Some of the most bizarre cadences of breathing those in which unwanted breaths intrude on speech or those characterized by incoordination of laryngeal closure, diaphragmatic movement, or swallowing or by respiratory tics have occurred in paraneoplastic brainstem encephalitis Similar incoordinated patterns occur in certain extrapyramidal diseases Patterns such as episodic tachypnea up to 100 breaths per minute and loss of voluntary control of breathing were, in the past, noteworthy features of postencephalitic parkinsonism In Leeuwenhoek disease, named for the discoverer of the microscope who described and suffered from the disease, there is a continuous epigastric pulsation and dyspnea in association with rhythmic bursts of activity in the inspiratory muscles a respiratory myoclonus akin to palatal myoclonus (Phillips and Eldridge) Two such cases in our clinical material followed in uenza-like illnesses and resolved slowly over months Cheyne-Stokes breathing, the common and well-known waxing and waning type of cyclic ventilation reported by Cheyne in 1818 and later elaborated by Stokes, has for decades been ascribed to a prolongation of circulation time, as in congestive heart failure; but there are data that support a primary neural origin of the dis-
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order, particularly the observation that it occurs most often in patients with deep hemispheral lesions of the cerebral hemispheres Another striking aberration of ventilation is a loss of automatic respiration during sleep, with preserved voluntary breathing ( Ondine s curse ) The term stems from the German myth in which Ondine, a sea nymph, condemns her unfaithful lover to a loss of all movements and functions that do not require conscious will Patients with this condition are compelled to remain awake lest they stop breathing, and they must have nighttime mechanical ventilation to survive Presumably the underlying pathology is one that selectively interrupts the ventrolateral descending medullocervical pathways that subserve automatic breathing The syndrome has been documented in cases of unilateral and bilateral brainstem infarctions, hemorrhage, encephalitis (neoplastic or infectious for example, due to Listeria), in Leigh syndrome, and recovery from traumatic Duret hemorrhages The issue of a loss of automatic ventilation as a result of a unilateral brainstem lesion has been addressed above The converse of this state, in which there is complete loss of voluntary control of ventilation but preserved automatic monorhythmic breathing, has also been described (Munschauer et al) Incomplete variants of this latter phenomenon are regularly observed in cases of brainstem infarction or severe demyelinating disease and may be a component of the locked-in state The congenital central hypoventilation syndrome is thought to be an idiopathic version of the loss of automatic ventilation (see Shannon et al) This rare condition begins in infancy with apneas and sleep disturbances of varying severity or later in childhood with signs of chronic hypoxia leading to pulmonary hypertension As mentioned on page 345, several subtle changes in the arcuate nucleus of the medulla and a depletion of neurons in regions of the respiratory centers have been found in this condition, but further study is necessary Neurologic lesions that cause hyperventilation are diverse and widely located throughout the brain, not just in the brainstem In clinical practice, episodes of hyperventilation are most often seen in anxiety and panic states The traditional view of central neurogenic hyperventilation as a manifestation of a pontine lesion has been brought into question by the observation that it may occur as a sign of cerebral lymphoma, in which postmortem examination has failed to show involvement of the brainstem regions controlling respiration (Plum) Hiccup (singultus) is a poorly understood phenomenon It does not seem to serve any useful physiologic purpose, existing only as a nuisance, and is typically not associated with any particular disease It may occur as a component of the lateral medullary syndrome (page 678), with masses in the posterior fossa or medulla, and occasionally with generalized elevation of intracranial pressure, brainstem encephalitis, or with metabolic encephalopathies such as uremia Rarely, singultation may be provoked by medication, one possible offender in our experience being dexamethasone Since the triggers of hiccup often seem to arise in epigastric organs adjacent to the diaphragm, it is considered to be a gastrointestinal re ex, more than a respiratory one A physiologic study by Newsom Davis has demonstrated that hiccup is the result of powerful contraction of the diaphragm and intercostal muscles, followed immediately by laryngeal closure This results in little or no net movement of air He concluded that the projections from the brainstem responsible for hiccup are independent of the pathways that mediate rhythmic breathing Within a single burst or run of hiccups, the frequency remains relatively constant, but at any one
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