Medical Image of the Week: Subarachnoid Hemorrhage

Figure 1. Axial CT of the head without contrast demonstrates a large subarachnoid hemorrhage in the basal cisterns and adjacent to the insular cortices (blue arrows).

Figure 2. Coronal CT angiogram of the head demonstrates a saccular outpouching of the anterior communicating artery (blue arrow) consistent with an aneurysm.

A 70-year-old lady with a past medical history of hypertension and dyslipidemia was brought in by her family members for evaluation of confusion and headache for 1 week. There was no history of recent trauma or falls. There was no known family history of aneurysm or sudden death. On examination, her blood pressure was 139/99 mmHg, heart rate 92 bpm, afebrile and respiratory rate was 13 breaths per minute. She was alert but only oriented to self. Pupils were symmetric and reactive to light. She was able to follow commands and power was symmetric in all limbs.

CT of the head without contrast showed diffuse subarachnoid and intraventricular hemorrhage with signs of raised intracranial pressure (Figure 1). Neurosurgery was consulted and she underwent emergent insertion of an external ventricular drain. Head CT post-ventriculostomy showed improvement in her ventricular dilatation. CT angiography was performed later and showed an anterior communicating artery aneurysm (Figure 2), thought to be culprit of her subarachnoid hemorrhage. Craniotomy with surgical clipping was performed. This was followed by improvement in her mental status.

The common presenting symptom of patients with subarachnoid hemorrhage is headache. They will classically describe it as "worst headache of my life". This can be accompanied by altered mental status, nausea, vomiting, or meningeal signs. Head CT without contrast should be obtained immediately if there is suspicion of subarachnoid hemorrhage. Studies have shown that head CT is extremely sensitive if obtained within 6 hours of clinical presentation but its sensitivity declines over time (1). Lumbar puncture should be performed if head CT is negative but there is strong suspicion of subarachnoid hemorrhage. A combination of negative head CT and lumbar puncture is sufficient to rule out subarachnoid hemorrhage in a patient presented with headache (2).

Kai Rou Tey¹, MD; Tammer Elaini², MD

¹Department of Internal Medicine, University of Arizona College of Medicine- South Campus and ²Department of Pulmonary, Critical Care, Allergy and Sleep University of Arizona College of Medicine

Tucson, AZ USA

References

1. Perry JJ, Stiell IG, Sivilotti ML, et al. Sensitivity of computed tomography performed within six hours of onset of headache for diagnosis of subarachnoid haemorrhage: prospective cohort study. BMJ. 2011;343:d4277. [CrossRef] [PubMed]
2. Perry JJ, Spacek A, Forbes M, et al. Is the combination of negative computed tomography result and negative lumbar puncture result sufficient to rule out subarachnoid hemorrhage? Ann Emerg Med. 2008 Jun;51(6):707-13. [CrossRef] [PubMed] 

Cite as: Tey KR, Elaini T. Medical image of the week: subarachnoid hemorrhage. Southwest J Pulm Crit Care. 2016;13(2):88-9. doi: http://dx.doi.org/10.13175/swjpcc063-16 PDF

Medical Image of the Week: Sleep Bruxism

Figure 1. Hypnogram and polysomnographic tracing showing an episode of rhythmic masticatory muscle activity (RMMA) during sleep. RMMA is defined when at least 3 consecutive EMG bursts (frequency 1 Hz) lasting greater than or equal to 0.25 seconds are scored on the masseter and temporalis channels.

Figure 2. Thirty second epoch of polysomnogram showing phasic sleep-bruxism during stage N2 sleep.

A 42 year-old man with a past medical history of insomnia, post-traumatic stress disorder, depression and both migraine and tension headaches was referred for an overnight sleep study. He had presented to the sleep clinic with  symptoms  of obstructive sleep apnea. Medications included sumatriptan, amitryptiline, sertraline, and trazodone. His sleep study showed: sleep efficiency of 58.2%, apnea-hypopnea index  of 33 events per hour, and arousal index of 14.5/hr. Periodic limb movement index was 29.2/hr. The time spent in the sleep stages included N1 (3.6%), N2 (72.5%), N3 (12.9%), and REM (10.9%). Figure 1 is representative of the several brief waveforms seen on his EEG and chin EMG. Sleep bruxism (SB) is a type of sleep-related movement disorder that is characterized by involuntary masticatory muscle contraction resulting in grinding and clenching of the teeth and typically associated with arousals from sleep (1,2).

The American academy of sleep medicine (AASM) criteria for sleep related bruxism diagnosis:

1. The patient reports or is aware of tooth-grinding sounds or tooth clenching during sleep.
2. One or more of the following is present: A. Abnormal wear of the teeth; B. Jaw muscle discomfort, fatigue, or pain and jaw lock upon awakening; and C. Masseter muscle hypertrophy upon voluntary forceful clenching.
3. The jaw muscle activity is not better explained by another current sleep disorder, medical or neurological disorder, medication use, or substance use disorder.

The exact etiology of SB is unknown. It is associated with sleep arousals, genetic factors, stress, anxiety and behavioral factors and medications like selective serotonin receptor inhibitors, tobacco, alcohol and recreational drug use and sleep disordered breathing (2).

The electromyogram (EMG) activity pattern in patients with SB is known as rhythmic masticatory muscle activity (RMMA) and involves the masseter and temporalis muscles in patterns of phasic and/or tonic contractions, most typically during stages N1 and N2 of sleep (2,3). Clinically, bruxism can result in abnormal tooth wear, masseter muscle hypertrophy, reduced salivation, and morning headaches (1,2).

Sleep bruxism has been shown to be strongly associated with tension and migraine headaches (4). Treatment of the underlying sleep disordered breathing with positive airway pressure may eliminate bruxism during sleep (5). Treatment involves oral appliances such as occlusal splints or mandibular advancement devices (2). There is insufficient evidence to support pharmacotherapy in the treatment of sleep bruxism (1).

Jared Bartell¹, Safal Shetty, MD^1,2, and John Roehrs, MD^1,2

¹University of Arizona Medical Center, Tucson, AZ

²Southern Arizona VA Health Care System, Tucson, AZ

References

1. Macedo CR, Macedo EC, Torloni MR, Silva AB, Prado GF. Pharmacotherapy for sleep bruxism. Cochrane Database Syst Rev. 2014;10:CD005578. [CrossRef] [PubMed] 
2. Carra MC, Huynh N, Lavigne G. Sleep bruxism: a comprehensive overview for the dental clinician interested in sleep medicine. Dent Clin North Am. 2012;56(2):387-413. [CrossRef] [PubMed]
3. Valiente López M, van Selms MK, van der Zaag J, Hamburger HL, Lobbezoo F. Do sleep hygiene measures and progressive muscle relaxation influence sleep bruxism? Report of a randomised controlled trial. J Oral Rehabil. 2014 Nov 21. [CrossRef] [PubMed]
4. De Luca Canto G, Singh V, Bigal ME, Major PW, Flores-Mir C. Association between tension-type headache and migraine with sleep bruxism: a systematic review. Headache. 2014;54(9):1460-9. [CrossRef] [PubMed]
5. Oksenberg A, Arons E. Sleep bruxism related to obstructive sleep apnea: the effect of continuous positive airway pressure. Sleep Med. 2002;3(6):513-5. [CrossRef] [PubMed]

Reference as: Bartell J, Shetty S, Roehrs J. Medical image of the week: sleep bruxism. Southwest J Pulm Crit Care. 2015;10(3):140-2. doi: http://dx.doi.org/10.13175/swjpcc016-15 PDF