POST EXAMINATION REPORT DATE

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Arron Osborne
5 years ago
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1 POST EXAMINATION REPORT DATE Regarding xxxx (DOB: xxxx). The patient has been struggling with severe fatigue, dyspnea, dysphagia, neck and temporomandibular pain for many years. He is also plagued by visual impairment, brachialgia, chest pain and other nagging symptoms. The patient states that his symptoms of fatigue have been reducing his quality of life since late adolescence, and throughout his adulthood, indicating longstanding underlying problems. Consistently, upon examination of the patient, it is my impression that this is a complex, multifactorial problem. The patient has several cranial nerve deficits revealed during neurological examination. He is light and sound sensitive, has nystagmus and diplopia toward the right. Periodic difficulty swallowing. There is atrophy of the masseter and temporalis muscles with poor contraction when biting (this may also be a TMD sequela). Morley s test and Pemberton s tests are positive, indicating thoracic outlet syndrome with subsequent cerebroarterial hyper perfusion (a consequence of distal subclavian compression) and intracranial hypertension. There is brachial weakness, most pronounced on the right side, where weakness of shoulder abduction (C5-6), wrist flexion (C6-7), elbow extension (C7-8), 1 st (C56) & 5 th (C8-T1) finger opposition and abduction are all weak, again compatible with TOS. Common symptoms of TOS are arm and chest pain, periscapular pain, dyspnea and tightness of the throat. Examination of the patient s CTCB images reveal severe narrowing of the atlantostyloid interval (ASI), likely obstructing the internal jugular veins bilaterally. There is 1mm and 3mm right/left intervals, respectively, which is very narrow (Gweon 2011). Mechanical obstruction of the IJVs at the ASI is a common occurrence (Jayaraman 2012), but little-known. It is mainly caused by poor cervical posture, where the patient hinges back at the upper neck, causing narrowing of the C1 transverse process and cranial styloid process, impinging the CN9-11 and internal jugular veins between them. Further, TOS (arterial hyperperfusion) in tandem with obstructed cerebrovenous drainage, is very unfortunate, and may lead to severe increase in intracranial pressures, likely explaining the patient s cranial nerve deficits and diffuse symptoms. Common symptoms of ICH are headache, fatigue, cranial nerve deficits such as diplopia, visual impairment, dysphagia, etc (Higgins 2017, Higgins 2015, Kincaid 2006, Jensen 2016, Mollan 2014, Larsen 2018c). In search of further evidence in support of raised intracranial pressure, a transorbital ultrasound examination was performed. In this regard, approximately 9 mm dilation of the optic nerve sheaths was demonstrated, with adherent papilledema. This is extremely high, and highly compatible with the patient s symptoms, and neurological examination. Research shows that an optic nerve sheath diameter > 5,8mm has high correlation with pathological increases in ICP (80% (Geeraerts 2008)). Doppler examination of the extracranial vessels was also performed. The systolic peaks of the internal carotid arteries are delayed, dampened and rounded, and the diastolic declination is faster than normal. Similar waveforms are seen in the vertebral arteries. There are thus abnormal waveforms of the carotid and vertebral arteries, compatible with cerebrovascular saturation (congestion) (Larsen, 2018c). Interestingly, the patient s waveforms are clearly abnormal despite a very low heart rate, indicating severe congestion. He frequently went below 50 bpm during the examination, consistent with bradycardia. It is known that patients with intracranial hypertension develop compensatory bradycardia in severe circumstances (Agrawal 2008), as this reduces arteriocerebral pressure, and I thus consider this finding to be a secondary effect of longstanding ICH. Based on the above, it is my impression that xxxx suffers from primary mechanical jugular stenosis and thoracic outlet syndrome, leading to secondary intracranial hypertension, myalgic encephalomyelitis. We have commenced conservative treatment of these problems, mainly aiming to broaden the atlantostyloid interval and to rehabilitate the scalenus muscles TRENING OG REHAB - Eikenga OSLO Post@treningogrehab.no

which are compressing his brachial plexus and subclavian vessels, causing TOS. With regards to the patient s jaw pain, he is already involved with several dentists and treatment of this problem.

2 which are compressing his brachial plexus and subclavian vessels, causing TOS. With regards to the patient s jaw pain, he is already involved with several dentists and treatment of this problem. The patient has been prescribed strengthening exercises for the pterygoid muscles on my behalf, to aid in decompression of the condyle and glenoid fossa. Finally, in light of the patient s extensive medical history and symptoms, I find it peculiar and somewhat worrisome that proper imaging has not been done. It is my opinion that MR images of the cervical spine and cerebrum should be obtained. With regards Kjetil Larsen Trainingandrehabilitation.com 1. Larsen K. Occult intracranial hypertension as a sequela of biomechanical internal jugular vein stenosis: A case report. Anaesth Pain & Intensive Care 2018;22(2): Geeraerts T, Merceron S, Benhamou D, Vigue B, Duranteau J. Noninvasive assessment of intracranial pressure using ocular sonography in neurocritical care patients. Crit Care. 2008;12(Suppl 2):P Higgins N, Trivedi R, Greenwood R, Pickard J. Brain slump caused by jugular venous stenoses treated by stenting: a hypothesis to link spontaneous intracranial hypotension with idiopathic intracranial hypertension. J Neurol Surg Rep Jul;76(1):e188 e193. [PubMed] [Free Full Text] doi: /s Jayaraman MV, Boxerman JL, David LM, Haas RA, Rogg JM. Incidence of Extrinsic Compression of the Internal Jugular Vein in Unselected Patients Undergoing CT Angiography. AJNR Am J Neuroradiol Aug;33(7): doi: /ajnr.A2953. Epub 2012 Feb Higgins JNP, Pickard JD, Lever AML. Chronic fatigue syndrome and idiopathic intracranial hypertension: Different manifestations of the same disorder of intracranial pressure? Med Hypotheses Aug;105:6-9. doi: /j.mehy Epub 2017 Jun Kincaid O, Rowin J. Intracranial hypertension causing polyradiculopathy and late or absent F-waves. J Neurol Neurosurg Psychiatry. 2006;77(12): Jensen RH, Radojicic A, Yri H. The diagnosis and management of idiopathic intracranial hypertension and the associated headache. Ther Adv Neurol Disord. 2016;9(4): Mollan SP, Ali F, Hassan-Smith G, Botfield H, Friedman DI, Sinclair AJ. Evolving evidence in adult idiopathic intracranial hypertension: pathophysiology and management. J Neurol Neurosurg Psychiatry. 2016;87:

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Occult intracranial hypertension as a sequela of biomechanical internal jugular vein stenosis: A case report

CASE REPORT ANAESTHESIA, PAIN & INTENSIVE CARE www.apicareonline.com Occult intracranial hypertension as a sequela of biomechanical internal jugular vein stenosis: A case report Kjetil Larsen, CES* *Corrective