Neurological Emergencies in Geriatric Patients


Key Points

  • Geriatric patients tend to have atypical presentation of diseases, and the signs and symptoms may be nonspecific, contributing to delayed diagnoses.

  • The incidence of intracerebral hemorrhage increases with age.

  • Advanced age has been identified as the strongest independent risk factor for cerebrovascular disease, and older adults tend to have worse outcome after stroke, with more stroke-related death, disability, and subsequent increased rates of dementia compared with younger stroke patients.

  • Epilepsy is most common in the elderly population due to increased risk factors such as prior stroke, trauma, and neurodegenerative disorders.

  • In cases of acute or progressively worsening mental status change, computed tomography of the head is an appropriate study, with follow-up magnetic resonance imaging of the brain in cases of identified pathology or suspected occult pathology, or to confirm a suspected clinical diagnosis.

  • In all patients with suspected central vertigo, imaging is a necessity, as the patient should be assumed to have an acute ischemic stroke until proven otherwise.

  • In patients with syncope, any suspicion for neurological injury based on the history and physical examination should prompt neuroimaging.

Introduction

The elderly population is the fastest-growing population group in the world, with an estimate of 71 million adults older than 65 years in the United States and 1 billion worldwide by the year 2030. Elderly patients are more likely to require emergency care, and the number of visits to the emergency departments continues to rise. Clinical evaluation in geriatric patients tends to be challenging, as signs and symptoms have low specificity and are less reliable than in younger patients. Furthermore, multiple comorbidities found in older patients may confound diagnoses. Elderly patients are prone to serious neurologic problems, with higher incidence of neurologic conditions such as stroke, hemorrhage, and epilepsy. The increased number of elderly patients, the higher incidence of neurologic conditions, and the clinical challenges faced with this population underscore the importance of neuroimaging in older patients. This chapter will discuss imaging findings of neurological emergencies in geriatric patients.

Intracranial Hemorrhage

Intracranial hemorrhage (ICH) is a growing cause of death and disability worldwide due to the increasing population of elderly people in the developed world. The incidence of intracerebral hemorrhage is 5.9 per 100,000 in ages 35 to 54 years, 37.2 per 100,000 in ages 55 to 74 years, and 176.3 per 100,000 in ages 75 to 94 years. Risk factors include falls, amyloid angiopathy, hypertension, and greater use of anticoagulant or antiplatelet therapy, with mortality rates as high as 50%.

ICH can be subdivided by location, either within the brain parenchyma or in the surrounding compartments, including the subdural, epidural, subarachnoid, and intraventricular spaces. ICH most commonly occurs in the setting of trauma in the elderly population, with falls accounting for 84% of trauma incidents in patients aged 65 years or older, and motor vehicle–related trauma being the second most common mechanism of injury.

Noncontrast computed tomography (NCCT) is the imaging modality of choice in the acute setting due to speed and high sensitivity for detecting ICH. NCCT helps guide the clinician to the etiology of the hemorrhage, assesses ICH evolution, evaluates for the presence of mass effect and shift of midline structures and hydrocephalus, and assesses bony integrity. Computed tomography (CT) angiography (CTA) and CT venography may be useful in the acute setting for the evaluation of arterial and venous vasculature when vascular lesions or vascular injury are suspected.

Although typically not the first imaging modality, magnetic resonance imaging (MRI) can also be used in the evaluation of ICH and has high sensitivity for intraparenchymal microbleeds. The presence of microbleeds may be a marker for underlying pathologies, including hypertension, amyloid angiopathy, vascular malformations, posttreatment changes, and diffuse axonal injury, and can help predict the risk of future bleeding events.

The appearance of blood on CT and MRI varies depending on the staging of blood products and the chemical state of hemoglobin ( Table 2.1 and Fig. 2.1 ).

Table 2.1
Hemorrhage Phases and Appearance on Computed Tomography and Magnetic Resonance Imaging
Hemorrhage Phase Time Computed Tomography Density a Hemoglobin Magnetic Resonance Imaging Signal a
T1 T2
Hyperacute <12 hours Isodense <1 hour, then hyperdense Oxyhemoglobin Isointense Iso- to hyperintense
Acute 12 hours–3 days Hyperdense Deoxyhemoglobin Iso- to hypointense Hypointense
Early Subacute 3–7 days Hyper- to isodense Intracellular methemoglobin Hyperintense Hypointense
Late Subacute 1–3 weeks Iso- to hypodense Extracellular methemoglobin Hyperintense Hyperintense
Chronic >3 weeks Hypodense Hemosiderin Hypointense Hypointense in parenchyma, Hyperintense (equivalent to CSF) if extraaxial
CSF , Cerebrospinal fluid.

a Relative to grey matter.

Fig. 2.1, Magnetic resonance imaging and noncontrast computed tomography (NCCT) images of hemorrhages at different stages. The first row (A–C) shows acute intraparenchymal hemorrhage in the right frontal lobe (arrows). Note isointense signal on T1-weighted imaging (WI) (A), hypointense signal on T2WI (B), and corresponding hyperdensity on NCCT (C). The second row (D–F) shows early subacute hemorrhage. Note hyperintense signal on T1WI (D) and hypointense signal on T2WI (E) in the left parietal lobe (white arrows), consistent with early subacute hemorrhage, with associated cavernous malformation (star). NCCT (F) on a different patient shows isodense attenuation along the left frontoparietal convexity, consistent with early subacute subdural hematoma (black arrow). The third row (G–I) shows late subacute hemorrhage. Note hyperintense signal on both T1WI (G) and T2WI (H) in the right occipital lobe (white arrows) consistent with late subacute intraparenchymal hemorrhage. Iso- to hypodense attenuation along the left convexity on NCCT (I) of a different patient is consistent with late subacute subdural hematoma (black arrow). There is associated midline shift (arrowhead). Fourth row (J–L) shows chronic subdural hematoma along the right frontoparietal convexity (arrows). Note hypointense signal on T1WI (J), hyperintense signal on T2WI following the signal of cerebrospinal fluid (K), and corresponding hypodensity on NCCT (L).

Subdural Hematoma

Subdural hematomas (SDHs) are the most common ICH in the elderly, most of them posttraumatic, with a reported annual incidence of 46.7 per 100,000 in ages 65 to 74 years. The relative risk for SDH is 5 times higher in the 75 to 84–year-old age group, and 13 times higher in those older than 85 years. Minor trauma can produce asymptomatic acute subdural hemorrhage, which then results in chronic SDH. These patients are also predisposed to acute bleeding within the chronic collection, resulting in acute on chronic SDH.

On imaging, SDHs are seen along the falx or tentorium, or appear as crescentic collections along the convexities within the subdural space, typically crossing suture lines ( Fig. 2.2 ).

Fig. 2.2, Different locations of acute subdural hematomas. Coronal noncontrast computed tomography (NCCT) (A) shows acute subdural hematoma along the left tentorial leaflet (long arrow) and left convexity (short arrow). Axial NCCT (B) shows subdural hematoma along the bilateral tentorial leaflets (long arrows) and the left temporo-occipital convexity (short arrow). Axial NCCT through the high frontal and parietal lobes (C) shows acute subdural hematoma along the falx bilaterally (arrows).

Epidural Hematoma

Epidural hematomas are relatively uncommon in the elderly population. Most epidural hematomas occur secondary to direct impact, with 80% to 95% of patients having a concomitant skull fracture. Some 90% of epidurals are arterial in nature, often involving trauma to the middle meningeal artery. The remaining 10% are venous in nature, resulting from trauma to a dural sinus.

On imaging, epidural hematomas have a classic hyperdense and biconvex appearance ( Fig. 2.3 ) and do not typically cross suture lines, unless there is a concomitant sutural diastasis. Compression of the adjacent brain parenchyma is often present.

Fig. 2.3, Epidural hematoma. Coronal (A) and axial (B) noncontrast computed tomography of the brain in a 77-year-old male after a fall demonstrate a biconvex hyperdense lesion centered along the right parietal convexity (arrows in A and B), consistent with epidural hematoma.

Subarachnoid Hemorrhage

Subarachnoid hemorrhage (SAH) is the most encountered type of traumatic ICH, and is typically seen in the cerebral sulci along the convexities and vertex of the head. Although MRI is less commonly used for initial evaluation of head trauma, the combination of fluid attenuation inversion recovery (FLAIR) and susceptibility-weighted imaging (SWI) sequences has excellent sensitivity for acute ICH and has been shown to be superior to CT in detecting acute SAH. Acute traumatic SAH is identified by hyperintense signal abnormality within the cerebral sulci on FLAIR sequences and hypointense blooming on SWI ( Fig. 2.4 ).

Fig. 2.4, Acute subarachnoid hemorrhage (SAH). Hyperdensity along the left frontal sulci on noncontrast computed tomography (A), with corresponding hyperintense signal on fluid attenuation inversion recovery (B) and susceptibility on susceptibility-weighted imaging (SWI) (C), is consistent with acute SAH (long arrows). Siderosis from chronic SAH (short arrow) is seen in the right frontal sulci on SWI (C).

Some 80% to 85% of spontaneous (i.e., nontraumatic) SAHs are caused by rupture of saccular aneurysms. Most saccular aneurysms occur at the circle of Willis and bifurcation of the middle cerebral arteries (MCAs); thus, most aneurysmal hemorrhages involve the basal cisterns and sylvian fissures ( Fig. 2.5 ). Once an acute SAH with a basal aneurysmal pattern is identified on initial NCCT, CTA is the indicated next step for identification of aneurysms. Aneurysmal hemorrhages commonly result in hydrocephalus and are associated with considerable morbidity and mortality. Although risk is not necessarily associated with increasing age, poor outcomes are associated with advanced age. Mortality from aneurysmal SAH approaches 35%, with 10% to 25% of patients dying before arrival at the hospital. Approximately one-third survive, but with disabling neurologic deficits, and only 30% return to independent living.

Fig. 2.5, Aneurysmal subarachnoid hemorrhage. (SAH) Axial (A and B) and sagittal (C) noncontrast computed tomography in a 67-year-old male with acute “worst headache of life” from ruptured anterior communicating artery aneurysm. Extensive SAH centered at the basal cisterns and adjacent sulci (long arrow). Note intraventricular hemorrhage with mild hydrocephalus (short arrow).

Intraparenchymal Hemorrhage

Traumatic

Acceleration and deceleration injury can result in cerebral contusions, which may be hemorrhagic or nonhemorrhagic. These commonly occur in areas closer to the skull base, including the anteroinferior frontal and temporal lobes. Contusions can occur at the site of impact and in a location directly opposite to the point of initial impact secondary to brain recoil, termed coup/contrecoup injury ( Fig. 2.6 ).

Fig. 2.6, Intraparenchymal hemorrhagic contusions in a 68-year-old male postfall. Axial (A and B) and sagittal (C) noncontrast computed tomography shows multiple cerebral contusions in the left temporal lobe and inferior left frontal lobe (long arrows) associated with scattered adjacent subarachnoid hemorrhage (short arrows).

Hypertensive

Hypertension is the most common cause of nontraumatic intraparenchymal hemorrhage among the elderly, and accounts for 40% to 50% of nontraumatic intraparenchymal hemorrhage. Hypertensive hemorrhages occur in typical locations, including the basal ganglia, thalami, pons, and cerebellum. The putamen/external capsule is the most common location and accounts for approximately two-thirds of all hypertensive intraparenchymal hemorrhages ( Fig. 2.7 ).

Fig. 2.7, Hypertensive intraparenchymal hemorrhage. Noncontrast computed tomography with axial (A), sagittal (B), and coronal (C) reconstructions shows a hypertensive intraparenchymal hemorrhage (long arrows) in the region of the left basal ganglia.

You're Reading a Preview

Become a Clinical Tree membership for Full access and enjoy Unlimited articles

Become membership

If you are a member. Log in here