Cheynes-Stokes Respiration in Acute Stroke
Cheynes-Stokes Respiration in Acute Stroke
Abstract & Commentary
By John J. Caronna, MD, Vice-Chairman, Department of Neurology, Cornell University Medical Center, Professor of Clinical Neurology, NewYork-Presbyterian Hospital. Dr. Caronna reports no financial relationship relevant to this field of study.
Synopsis: Recent imaging studies reinforce the classical concept that periodic breathing in acute stroke indicates a large supratentorial infarct or hemorrhage.
Source: Rowat AM, et al. Abnormal breathing patterns in stroke: relationship with location of acute stroke lesion and prior cerebrovascular disease. J. Neurol Neurosurg Psychiatry. 2007;78:277-279.
Periodic breathing (PB) is an abnormal pattern of respiration in which cyclic increases in the rate and depth of breathing alternate with a reduction or complete cessation of respiratory effort. Most clinicians use the term Cheynes-Stokes Respiration (CSR) to denote crescendo-decrescendo breathing. The causes of PB include pulmonary disease, cardiac failure, and neurogenic disturbances of respiratory control. In 1980, Plum and Posner1 stated that CSR implied bilateral dysfunction of deep structures in the cerebral hemispheres and diencephalons. They observed, however, that in reports where CSR was associated with structural brain lesions, the sites of damage found at autopsy ranged widely from the forebrain to the rostral pons. In their experience, the emergence of CSR in patients with supratentorial mass lesions sometimes provided a valuable sign of incipient transtentorial herniation. More recent studies have failed to find any association between CSR and the location of brain lesions on imaging studies.2
Rowat and associates sought to determine in acute stroke patients whether PB is associated with acute involvement of any particular part of the brain or with the extent of total damage. In 134 patients with acute stroke, breathing pattern was recorded using portable continuous monitoring equipment. Patients underwent either CT or MRI scanning of the brain. A neuroradiologist blind to breathing patterns and clinical results classified the acute stroke lesions and prior cerebrovascular disease on brain images.
PB was identified in 31/134 (23%) of acute stroke patients. In these patients, there were 26 ischemic infarcts and 5 intracerebral hemorrhages. Twenty-eight acute lesions were supratentorial and 3 were infratentorial in location. There was no relationship between PB and either unilateral or bilateral lesions in any discrete brain location. PB was associated with large acute hemisphere strokes rather than small or medium-sized ones (p = 0.01) and with strokes causing severe rather than no or only mild mass effect (p = 0.03). There was no association between PB and severe prior cerebrovascular disease on brain imaging.
The authors concluded that PB is related to acute, not old, strokes, particularly to large acute hemisphere lesions with mass effect.
Commentary
Breathing is a vital function that is integrated by nervous influences that arise from nearly every level of the brain and upper spinal cord. It is not surprising, therefore, that Rowat and associates found no specific PB-associated "respiratory center" in the brain. It should be noted that the present study was limited because it relied mainly on CT imaging and, therefore, it is possible that damage to small brain areas, especially those in the brainstem, was undetected.
That PB is associated with large supratentorial lesions that cause brain shift agrees with the pre-CT and pre-MRI era observations of Plum and Posner.1 It may be in such cases that increased intracranial pressure or herniation stimulates efferent sympathetic vasoconstrictor pathways triggering pulmonary edema and cardiac failure that produce PB. If so, central or "neurogenic" PB would reflect cardiopulmonary dysfunction as well as brain damage.
The present study has not clarified the relationship of brain damage to CSR. It does, however, reaffirm the value of clinical observation of breathing pattern in acute stroke.
References:
1. Plum F, Posner JB. The Diagnosis of Stupor and Coma. 3rd Edition. FA Davis, Philadelphia 1980.35-36.
2. Nachtmann A, et al. Neurology. 1995; 45:820-821.
Recent imaging studies reinforce the classical concept that periodic breathing in acute stroke indicates a large supratentorial infarct or hemorrhage.Subscribe Now for Access
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