THE CLINICAL CHALLENGE
Neurologic conditions are typically diagnosed and managed in the outpatient setting. Many of the diagnostic tests that are staples of neurologic practice are difficult to access or simply not accessible in the emergency department (ED). Although magnetic resonance imaging (MRI) is becoming more available, it is time-consuming, often not appropriate in stable chronic complaints, and unsuitable for an unstable patient. Electroencephalogram (EEG), neuromuscular testing, and much of the autoimmune-focused blood work are generally not available in a timely fashion. Nevertheless, patients with neurologic conditions frequently present to the ED with an exacerbation or progression of their disease; thus, the emergency clinician must be familiar with stabilization strategies. Even if the diagnosis is beyond the purview of the emergency clinician, discovering and documenting neurologic deficits can greatly assist clinicians in the future in establishing symptom chronicity and correlating progress with diagnostic testing and treatments.
Transverse myelitis is a poorly understood condition characterized by acute spinal cord dysfunction below the level of a spinal cord lesion. Given its location and chronicity, transverse myelitis can mimic a compressive spinal cord lesion. Although transverse myelitis is thought to be inflammatory, it is unclear whether the trigger is autoimmune, infectious, or paraneoplastic. More likely, it is a heterogeneous syndrome with multiple possible etiologies.5
Diagnosis is usually made with MRI, and treatment is aimed at addressing the underlying inflammation, with corticosteroids being the mainstay of acute management.6
POST STROKE SYNDROMES
Although stroke in the ED is typically considered in the context of acute presentation, there is an equally concerning chronic component. Brain tissue damaged in a stroke does not heal. Once infarcted, the tissue dies and becomes nonfunctional; even in the absence of revascularization, stroke deficits can improve or completely resolve. The process of overcoming these deficits requires the brain to adjust for the lost function rather than replace it. Neurologic function is transferred to other cells, and this “rewiring” can allow the deficit to improve.
The importance of this rewiring comes in the face of a second, often nonneurologic insult. When faced with another challenge, such as infection or sleep deprivation, the brain can decompensate and allow the stroke deficit to emerge again or worsen. Termed recrudescence
recapitulation of old stroke deficits should prompt the clinician to look beyond stroke. Indeed, it is unlikely that the patient has a new infarct that exactly matches the neuroanatomy compensating for the old deficit. It is more likely that another process, such as occult infection, is causing the patient’s brain to re-exhibit the old stroke pattern. Recrudescence must be differentiated from an acute stroke, and treatment should be focused on the acute process rather than anchoring on the neurologic deficit.
TABLE 9.1 Common Drugs Used to Treat Spasticity
Usual Dose Range
Common Side Effects
5-10 mg tid
Nausea, confusion, headache, weakness, dizziness
Central acting α-2 agonist
2 mg qhs
Drowsiness, hypotension, dry mouth
2 mg bid
Inhibition of Ca release in peripheral muscle cells
25 mg daily-tid
Flushing, drowsiness, headache
Skeletal muscle relaxant
500 mg qid
bid, twice a day; Ca, calcium; GABA, gamma-aminobutyric acid; qhs, every night at bedtime; qid, 4 times a day; tid, 3 times a day.
In addition to recrudescence, many patients present with complications of stroke-related disability. Weakness can precipitate falls. Swallowing impairment can lead to aspiration. Patients with strokes sometimes present with pain that is thought to be a centrally mediated variant of complex regional pain syndrome (CRPS; see section that follows).7
POST SPINAL CORD INJURY
Emergency clinicians are familiar with the acute management of spinal cord trauma. However, many clinicians are less familiar with the chronic complications of the same injuries. Patients with spinal cord injuries face numerous chronic problems associated with the repercussions of spinal cord injury and paralysis. In the weeks and months following spinal cord injury, blood pressure often drops and orthostasis is common. This is likely a result of muscle atrophy and paralysis. These symptoms usually level off as unused muscles become spastic and systemic circulation adjusts.
Coronary artery disease is an often-underappreciated component of spinal cord injury. It may be 3 times higher in patients with spinal cord injury than in the general population.8
This is likely caused by poor mobility and reduced capacity for aerobic exercise. Accordingly, spinal cord injury should be viewed as an independent risk factor when evaluating a patient with chest pain.
Immobility can become even more pronounced as patients with spinal cord injury become older. Beyond the usual changes associated with aging, such as osteoarthritis, patients with spinal cord injury are far more likely to develop heterotopic bone formation, further limiting joint motion. Some degree of heterotopic ossification is seen in 20% of patients with traumatic brain injury/spinal cord injury.9
It can exacerbate the direct consequences of paralysis and further disable the patient.
Spinal cord injury above the diaphragm can impair ventilation by weakening the chest wall and accessory muscles. This likely contributes to the development of atelectasis and pneumonia. A long-term study that followed patients up to 20 years post injury found that pneumonia was the third most common complication after pressure ulcers and autonomic dysreflexia.10
Spasticity with pain is a frequent complication of spinal cord injury. It is likely the consequence of reduced inhibitory neurostimulation. Although the result is often painful muscle contraction, spasticity also helps increase venous return and maintain blood pressure in a paralyzed patient. Table 9.1
provides a list of medications used to treat spasticity and the acute discomfort it causes.
Most patients with spinal cord injury, even those with incomplete injuries, have some degree of bladder impairment. Lesions that are lower in the cord or cauda equina tend to produce bladder flaccidity, and these patients have trouble with voiding. Higher lesions may result in bladder spasms resulting in ongoing discomfort and difficulties with continence. Sphincter dysfunction can also impair bladder emptying. Patients with spinal cord injury may be unable to sense when their bladders are full, and in rare cases, this can produce a profound vagal reaction and hypotension.
The tools used to treat bladder dysfunction carry their own risks. Many patients with spinal cord injury use catheter devices either intermittently to facilitate continence or as chronic indwelling devices for ease of care. As with any introduction of a foreign body into a sterile space, these devices carry a higher risk of infection. Urosepsis should be high on the differential for a post-spinal cord injury patient presenting with shock.
COMPLEX REGIONAL PAIN SYNDROME
CRPS is a disorder that is characterized by chronic localized pain out of proportion to, or in the absence of, an inciting event. CRPS is divided into two main categories: CRPS type 1 encompasses cases without an obvious peripheral nerve injury (roughly 85% of cases) and CRPS type 2 is defined as CRPS with a clear mechanism for peripheral injury such as a crush injury or operation (15% of cases).11
The primary manifestation of CRPS is chronic, often extreme pain more commonly found in a patient’s upper extremity. Sensory disturbances in a peripheral nerve distribution may also be present. Roughly two-thirds of CRPS patients have functional motor weakness related to pain. Autonomic symptoms, such as skin color changes, skin temperature changes, or sweat production may also be present. The cause of CRPS is unknown. Historically, theories have focused on nerve injury and the potential for a “short circuit” in nerve conduction. This type of explanation seems less probable, given that many CRPS patients have no inciting injury. More recent research has found elevated levels of inflammatory cytokines in CRPS patients, leading to the hypothesis that local release of pain mediating peptides may be the underlying etiology.12
Although no curative treatment exists for CRPS, rehabilitation and analgesia are the mainstays of management. In the acute setting, a patient may present with pain out of proportion to any physical findings. There is no diagnostic test for CRPS; thus, acute management is focused on ruling out correctable causes, for example, necrotizing fasciitis, compartment syndrome, and acute limb ischemia, all of which can present with extreme pain in a relatively normal-appearing limb. In a patient with known CRPS, management of acute pain should focus on providing analgesia, encouraging motor function, and ensuring follow-up that provides both physical therapy and chronic pain treatment (see evidence
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