A Case of Dizziness After Traumatic Cervical Spinal Cord Injury

PATIENT INFORMATION Ms. P, a 77-year-old woman, was working in her garden when she fell forward, hitting her head on concrete, and was immediately unable to move her arms or legs. Paramedics brought her to the hospital where computed tomography showed an acute, stable fracture of C1, and magnetic resonance imaging showed an abnormal signal intensity at C4–5 concerning for acute spinal cord injury (SCI). Her injury was managed conservatively with a cervical spine collar, and she was discharged to an inpatient SCI rehabilitation hospital 4 wks later. Before her injury, Ms. P was medically well, living independently with her husband. Her medical history was significant for hypothyroidism and 2 previous myocardial infarctions. On admission to rehabilitation, Ms. P reported bilateral hand numbness and weakness and mild lightheadedness with standing. Neurological examination showed C3 ASIA Impairment Scale D, motor functional incomplete tetraplegia. Sensation to light touch and pinprick was altered in a patchy distribution in the upper and lower limbs. Motor examination showed a central cord syndrome with weakness in the upper limbs and normal strength in the legs. On the left, power was grade 4/5 in the finger flexors and finger abductors. On the right, power was 4/5 in the elbow extensors and 2/5 in the finger abductors. One week after admission, Ms. P complained of sudden onset dizziness while having her neck massaged in supine. These symptoms lasted 15 to 20 seconds. When she sat up, the symptoms recurred. She felt the room spinning and felt as if she was falling to her right side. Her therapist noted that she appeared pale. There was no associated chest pain, palpitations, or shortness of breath. She did not complain of aural fullness, hearing loss, or tinnitus, and there was no new weakness, numbness, diplopia, headache, or dysarthria. Because of the sudden and severe nature of her symptoms, she was transferred to the emergency department. What is your differential diagnosis for dizziness and what serious diagnoses do you need to rule out? What would you look for on physical examination? CLINICAL FINDINGS The differential diagnosis for dizziness is extensive and can be divided into vertiginous and nonvertiginous causes (Table 1). Vertigo can be further divided into either central or peripheral causes. With such a broad differential, a thorough physical examination including cardiac and neurological examinations are essential. TABLE 1 - Differential diagnosis for dizziness Vertiginous Nonvertiginous Central Peripheral Stroke (including cerebellar and lateral medullary infarcts) Transient ischemic attack Vertebral or carotid artery dissection Vertebrobasilar insufficiency Migrainous vertigo Multiple sclerosis Benign paroxysmal positional vertigo Meniere’s disease Labyrinthitis Vestibular neuronitis Arrythmias Aortic stenosis Vasovagal syncope Orthostatic hypotension Metabolic disorders (eg, hypoglycemia) Panic disorder Autonomic dysreflexia On physical examination, vital signs were as follows: temperature, 36.7°C; heart rate, 63–67 bpm; oxygen saturation, 97%; and blood pressure (BP), 134/60 mm Hg (lying), 128/59 mm Hg (sitting), and 98/48 mmHg (standing). Neurological examination was unchanged from previous and no focal cranial nerve deficits including no nystagmus were found. Cardiorespiratory examination was unremarkable. A modified Dix-Hallpike maneuver (Fig. 1) showed vertical nystagmus.FIGURE 1: A–C, Modified Dix Hallpike test for diagnosis of BPPV. A, Patient sits on the examination table with legs straight in 30 degrees of Trendelenburg. This aims to accommodate the requirement of 30-degree neck extension at the end of a traditional Dix-Hallpike test. The clinician supports the patient’s neck in neutral, and the patient can hold onto the clinician’s arms for support. A second person should stand at the other side of the table to ensure smooth movement and safety throughout the test. B, The patient’s trunk is turned 45 degrees toward the side to be tested keeping the neck in neutral (in contrast to the traditional Dix-Hallpike test, which requires 45 degrees of neck rotation). C, The patient is then brought down in a controlled descent with the help of the second person such that 45 degrees of trunk rotation is maintained. The clinician observes the patient’s eyes for nystagmus. Note: The “patient” in the picture is portrayed by author CPS.What is your differential diagnosis for Ms. P and what is the most likely diagnosis? What investigations would you order? DIAGNOSTIC ASSESSMENT Based on the history and physical examination, Ms. P’s dizziness was most likely vertiginous due to the description of the room spinning and the positive Dix-Hallpike maneuver. The cause of her vertigo was unlikely central as her neurological examination was unchanged, but investigations were required to rule out potentially serious diagnoses. She also had an orthostatic drop in her BP, which is a nonvertiginous cause of dizziness and may have been contributory. To assess for central causes of vertigo, computed tomography and computed tomography angiography were performed. They demonstrated no acute intracranial pathology and no dissection in the extracranial carotid or vertebral arteries. If she had carotid artery atherosclerosis, neck massage may have resulted in diminished blood flow causing her symptoms. There was no significant large artery atherosclerosis. Given Ms. P’s cardiac history, an acute cardiac event needed to be ruled out. She had no cardiac symptoms, her troponin was not elevated, and her electrocardiogram was unchanged from previous making the likelihood of a cardiac event low. Systemic illness causing hypovolemia was unlikely the cause of her orthostatic hypotension given the laboratory investigations that showed the following: hemoglobin, 121 g/l; white blood cells, 3.2 × 109/l; creatinine, 66 umol/l; sodium, 143 mmol/l; potassium, 4.2 mmol/l; and serum glucose, 6.9 mmol/l. After the investigations, peripheral vertigo and orthostatic hypotension remained the most likely diagnoses. The vertiginous symptoms were consistent with benign paroxysmal positional vertigo (BPPV). The BPPV, an inner ear disorder, is characterized by brief episodes of vertigo associated with head movements and positionally induced nystagmus.1 The BPPV is a clinical diagnosis. A thorough history should differentiate between different causes of peripheral vertigo and assess for central causes and nonvertiginous causes of dizziness (Table 1). A Dix-Hallpike maneuver that induces vertical nystagmus supports the diagnosis of BPPV.1 Ms. P had a significant orthostatic drop in her BP, defined as a systolic BP drop of at least 20 mm Hg or a diastolic BP drop of at least 10 mm Hg within 3 min of standing.2 This may have explained the light headedness upon standing she initially reported and the symptoms when she sat up from supine. Causes for orthostatic hypotension include medications (eg, antihypertensives, sedatives, antidepressants, anticholinergics), neurogenic (eg, SCI, Parkinson disease, dementia with Lewy bodies), peripheral autonomic neuropathy (most commonly associated with diabetes), hypovolemia (either absolute as with diarrhea or relative as with heart failure), and deconditioning.3 Ms. P’s orthostatic hypotension was likely due to both her SCI and deconditioning. How would you manage BPPV? What is your approach to managing orthostatic hypotension in SCI? THERAPEUTIC INTERVENTION The initial treatment of BPPV should include canalith repositioning procedures such as the Epley maneuver.1 These procedures move the patient through specific body positions designed to relocate dislodged particles within the inner ear.1 Clinicians offered a modified canalith repositioning procedure (Fig. 2), but the patient declined as her symptoms were improving. Ms. P was also offered a trial of betahistine but declined. Pharmacologic management with vestibular suppressant medications such as benzodiazepines and antihistamines is not routinely recommended for the treatment of BPPV because of potentially harmful side effects.1FIGURE 2: A–D, Modified canalith repositioning technique for treatment of BPPV. Each position is maintained for 1 min. A, The patient lies on an examination table with the head piece tilted 30 degrees downward and a pillow placed under the opposite shoulder/trunk such that patient’s trunk is rotated 45 degrees toward the affected side. This aims to accommodate the requirement of 30 degrees of cervical extension and 45 degrees of cervical rotation in the traditional procedure. The clinician provides support to the patient’s neck and ensures that it is in neutral position. B, The pillow is removed, and the patient is turned away from the affected side and faces up. C, The clinician turns the patient 90 degrees further away from the affected side with the neck supported in neutral position. A helper turns the lower part of the body to align with the torso and bends the knees. D, The clinician turns the patient 45 degrees further away from the affected side with the neck supported in neutral position such that the patient can see the floor. Similarly, the helper facilitates turning of the hip and legs. Upon completion, the helper assists the patient to put the legs down and both clinician and helper assist patient to sit up at the edge of the table making sure that the neck is kept in neutral during the movement. Note: The “patient” in the picture is portrayed by author CPS.To treat Ms. P’s orthostatic hypotension, pregabalin was stopped (prescribed for neuropathic pain), and she was given compression stockings and an abdominal binder. She was also prescribed midodrine 2.5 mg orally daily in the morning. Midodrine is a selective α-1 adrenoreceptor agonist, which increases peripheral resistance. Its half-life is approximately 4 hours and increases BP for approximately 2–3 hours. Fludrocortisone, a potent synthetic mineralocorticoid, is also used to treat orthostatic hypotension3; however, there is limited evidence of its efficacy in SCI.4 FOLLOW-UP AND OUTCOMES Ms. P continued to have brief episodes of vertigo, often triggered by turning over in bed. At the time of discharge, 3 mos after her initial injury, her symptoms had significantly improved in intensity and duration. Ms. P tolerated the use of compression stockings and an abdominal binder, and her symptoms of orthostasis improved. She was discharged home, independent in mobility and her activities of daily living. DISCUSSION In approaching this patient presenting with dizziness, our strengths included a thorough history and physical examination. This was essential as the differential diagnosis was broad. Limited access to diagnostic testing is a challenge of working in an independent rehabilitation facility, and transferring a patient to the emergency department is often the only option to complete a timely workup to rule out potentially serious diagnoses. In retrospect, had we diagnosed orthostatic hypotension on admission, we could have implemented conservative management earlier. Overall, we believe that Ms. P had an appropriate workup for her symptoms and was offered treatment as per standard clinical practice. Dizziness is a common symptom in rehabilitation and requires a thorough history, physical examination, and targeted investigations to determine its etiology. In SCI, BPPV and orthostatic hypotension are common causes of dizziness. Left untreated, these conditions can have a significant impact on patients’ independence and participation in rehabilitation. Orthostatic hypotension is routinely managed by specialists in physical medicine and rehabilitation and is reviewed in detail elsewhere.4 Benign paroxysmal positional vertigo is also common after traumatic SCI but receives much less attention. A study of 62 consecutive patients with traumatic SCI admitted to inpatient rehabilitation found that the incidence of BPPV was 14.5%,5 which is much higher than the lifetime prevalence of 2.4% in the general population.6 Patients with cervical SCI were 2.87 times more likely to have BPPV compared with patients with thoracic or lumbar SCI. In cervical spine trauma, it is postulated that force is transmitted from the neck to the utricle in the inner ear, causing dislodgement of debris and leading to the development of BPPV.5 Modified techniques for the diagnosis and management of BPPV for patients in cervical collars (Figs. 1, 2) were shown to be safe and effective, and most patients’ symptoms resolved with one treatment maneuver.5 The literature on BPPV after traumatic SCI is otherwise quite sparse. A case report published in 2018 described the successful treatment of a patient with C3 complete tetraplegia who developed BPPV in the intensive care unit.7 An increased incidence of BPPV has also been reported in the head injury population,8 likely because of the same proposed etiology as cervical SCI. Specialists in physical medicine and rehabilitation and other rehabilitation health care practitioners should be familiar with the diagnosis and management of BPPV and orthostatic hypotension. This study conforms to all American Journal of Physical Medicine & Rehabilitation Resident Fellow Section CARE guidelines and reports the required information accordingly (see Supplemental Checklist, Supplemental Digital Content 1, https://links.lww.com/PHM/A974). INFORMED CONSENT The patient provided informed consent for the publication of this case.

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