INTRODUCTION: Cheyne-Stokes respiration (CSR) is a form of central sleep apnea that is quite distinct, with a crescendo-decrescendo ventilatory pattern with a central apnea or hypopnea at the nadir. The etiology of this disorder has never been fully understood. Our case suggests that cervical stenosis should be considered as a possible cause.
CASE PRESENTATION: Our patient was a 55-year-old woman who presented with 9 months history of hypersomnolence, fatigue, and nonrestorative sleep. Her spouse described “tremors and kicks while sleeping”. On review of systems she complained of new and severe daily headaches, poor concentration, memory problems, neck pain with radiation to shoulders, urinary hesitancy and depression. There was no history of snoring, weight gain, restless legs, or symptoms suggestive of narcolepsy. Past medical history was significant for: Cervical disc disease, dyslipidemia, depression, hypothyroidism, viral meningitis 10 years prior without sequelae, and pancreatitis secondary to gallstones. Medications included: Atorvastatin, Paroxetine, Fluoxetine, Levothyroxine, Metoprolol, Lorazepam, Oxycontin, and Propoxyphene. Social and family history were unremarkable. Physical examination revealed stable vital signs, BMI 33, neck circumference 14 inches, Mallampati class II airway, mildly hyperreflexic on deep tendon examination (3+) bilaterally, rest of the physical exam was normal. Arterial bloog gas showed a PH:7.39, PCO2:45, and PO2:67 on room air. Overnight polysomnegram (PSG) documented central apneas with CSR (AHI was 70 and 40 on two separate occasions). Brain MRI with contrast was normal. Extensive cardiac work up, including right and left heart catheterization was also normal. Treatment and interventions included CPAP and BIPAP, without clinical improvement. Other therapeutic interventions included Theophylline with subjective improvement but patient developed nausea and had to be discontinued. Trials of increased dead space (6 and 12 inches), and Acetazolamide were not helpful. MRI of the neck was performed and revealed; severe, multi level degenetrative joint and disc disease causing cord deformity requiering surgical C3-C7 foraminectomy with posterior fusion. The patient had a remarkable recovery from her symptoms. Overnight oximetry study performed after surgery was normal and without any changes usually found with CSR.
DISCUSSIONS: Ventilatory control is dependent on both metabolic (chemoreceptors, baroreceptors), as well as behavioral (wake-dependent) control systems. During sleep ventilation is critically dependent on the metabolic control system (via Po2 and Pco2 levels). Central sleep apnea (CSA) is the cessation of breathing during sleep in association with the absence of ventilatory effort. While CSA syndromes are heterogeneous, CSR is a distinct group with its typical crescendo-decrescendo ventilatory pattern and central apneas/hypopneas. The mechanisms involved in CSR remain poorly understood but the syndrome is well described in congestive heart failure, and patients with neurologic diseases. Our patient had the typical CSR pattern and underwent an extensive work up in an attempt to explain this abnormality. We hypothesize that in this case the severe cervical stenosis, and the impressive clinical response after surgical correction, suggest that cervical abnormalities (e.g. stenosis, compression…), should be considered in the list of causes of CSR. Several reports are found in the literature describing sleep disorders in patients with craniovertebral malformations, cervical spine surgeries, cervical trauma patients, and rheumatoid arthritis patients complicated with cervical and temporomandibular lesions.
CONCLUSION: Cervical spine lesions such as stenosis, and malformations from disc disease or other joint diseases can be associated with CSR and sleep disordered breathing through unknown mechanisms. Surgical therapy may lead to improvement or total resolution.
DISCLOSURE: Tarif Smadi, None.