Examining Neurocritical Patients

© Mayo Foundation for Medical Education and Research, under exclusive license to Springer Nature Switzerland AG 2021

E. F. M. WijdicksExamining Neurocritical Patients https://doi.org/10.1007/978-3-030-69452-4_1

1. Taking a History

Eelco F. M. Wijdicks¹  

(1)

Saint Marys Hospital, Mayo Clinic, Rochester, MN, USA

Eelco F. M. Wijdicks

Email: [email protected]

Keywords

System reviewPresentationIllnessTrajectory

What happened here? – is precisely what we will say (or think) while walking into a patient room and catching sight of a patient in neurologic distress. We might find ourselves in the emergency room with the intake nursing staff, at a rapid-response call with a resuscitating team, or in an intensive care unit (ICU) with the flight crew as the patient is transferred from a gurney. An established component of the neurocritical medical evaluation is, of course, taking a history (known also as anamnesis). This is not so easily done in an emergent or neurocritical setting. We will soon find out that others have asked the same question. Who will toil through the story? It is a formidable task, especially when patients are confused, aphasic, or, worse, sedated and intubated. The information-seeking healthcare provider relies on accompanying persons (ideally, close family members), but they often must travel separately, arriving in most instances after the patient enters the intensive care unit or the emergency room.

Frankly, these venues in no way resemble the outpatient setting in which the neurologist quietly greets the patient in the waiting room and leads him or her (an alert, fully aware individual) to a comfortable clinic office for a quiet, uninterrupted intake session. The ambience of the emergency room or the Neuro-ICU is often semi-chaotic, and the recounting of the circumstances of the event mostly falls to others. Furthermore, the narrative of the ictus and clinical trajectory may understandably be somewhat emotive. We will miss important points; they accumulate quickly in the heat of the moment.

Although a staple of our professional evaluation, it has been short changed in medical (and most certainly surgical texts). Few books address clinical history-taking in critically ill patients and none, I believe, at length. We rarely have the opportunity to have the patient describe the problem in his or her words. However, data-driven intensivists cannot rely on an incomplete history of chief complaints and its trajectory; they should make the effort to start from square one if information is muddled or contradictory.

Here’s the thing. A clinical history consists of determining the onset of symptoms, which symptoms are absent, how severe they were, how they were perceived, and how the symptoms progressed. Taking a history is what we should do first according to educational dogma. This is only partly true. We see patients at arrival and get a first clinical impression, some snippets of what happened, and sometimes even a report from the flight crew. These pieces of information, after a patient is stabilized or resuscitated, are barely enough, and we will seek more from arriving family members or the patient. Clinical history thus never can be fully isolated as a separate task, and we will be influenced by what we see and hear.

This opening chapter addresses all aspects of the medical history: the obstacles, competencies, and recognition of a clinical trajectory from onset to presentation. Examples of the value of a good medical history are shown but also the familiar biases, prejudices, and potential for lost focus and digression when asking questions. The closing chapter is how we communicate all of this and how we prioritize information. We can decry the loss of clinical skills with some justification, but even the most skilled clinical neurointensivist must work from a solid history that includes major tenets such as chief complaint, history of present illness, past medical history, family history, and social and occupational history.

Obstacles and Competency

Obtaining a reliable history requires the collaboration of a bystander (ideally) or a close family member. Summarizing a medical history for the first time places a tremendous burden, often underappreciated by clinicians, on witnesses, who may be derided as poor historians. This label is applied when families or patients provide vague descriptions, imprecise explanations (doctor so-and-so said), and mixed-up timelines. Moreover, neurologists should recognize that families may understand and define medical vocabulary differently. They may use words like numbness to describe weakness, that so-called seizures may actually be vasovagal collapse, and that confusion may be aphasia. More than in non-acute neurologic settings, families are overwhelmed with impaired observational skills. While this, in itself, often causes significant communication lapses, the situation may be further complicated by language and ethnic barriers and communication styles. Unfortunately, the hectic ICU environment may create an additional obstacle to rational explanations. The time needed for a carefully reconstructed timeline is infrequently available; essential information might only be recalled later. Particularly worrisome is the current cut-and-paste environment of electronic records and histories that are never questioned or confirmed.

A patient’s history as presented in a handoff may be too easily accepted, even when generated in an environment of continuous interruptions. Moreover, miscommunication-related medical errors have been linked to handoffs with communication interruptions [1, 2]. Interruptions lead to poor recall and disagreement about the importance of communicated information. (See Chap. 12 for a more comprehensive analysis of communication problems.)

No scale in neurology takes the patient’s history into account. In addition, there is little training in how to recognize cues with attentive listening, how best to communicate, how to avoid distractions in an urgent environment, and how to ask open-ended questions. Errors of commission, as these are known in legal circles, include trusting faulty memory, obtaining erroneous information, and failing to resolve contradictory statements in records or to review prior medical records. Urgent cases require quick histories, but thorough information-gathering (and, if needed, correctives) should come later, when the dust has settled. We tend to forget and move on to the next patient.

Experience is the best teacher on how to take a good history—knowing what to ask and how to redirect when needed. It also requires discernment about what can be ignored or minimized and what is crucially important. It is important to get a clear insight into what has happened, and some suggestions are shown in Table 1.1. Several elements of the history are critical, such as the onset and progress of symptoms. Clinical history can then be further deconstructed looking at more specifics (Table 1.2). Precipitating factors should be considered. For example, drug overdose must be considered in comatose patients with a normal computed tomography (CT) brain and for whom there are no neurologic signs other than coma. In addition to prescribed medications, neurointensivists must consider (and test for) other medications or drugs to which the patient might have had access. Patients with myasthenic crises virtually all had a precipitating infection. Guillain–Barré usually develops initially with symptoms that mimic an upper respiratory infection or a gastrointestinal complaint followed by (bloody) diarrhea. Neuromuscular respiratory failure often is worse at night because of a change to a supine position that precipitates diaphragmatic weakness.

High-pressure headaches are worse in the morning and have been attributed to a rise in intracranial pressure (ICP) during the night as a consequence of reclination, mild hypercarbia during sleep caused by respiratory depression, or a decreased cerebrospinal fluid (CSF) absorption. Low-pressure headache worsens with standing, coughing, sneezing, and exertion.

Table 1.1

Acute neurohistory in five numbers

Table 1.2

Deconstructing a clinical history

AVM arteriovenous malformation, CPR cardiopulmonary resuscitation, ED emergency department

Biases and Pattern Recognition

There are situations in which the team looks at magnetic resonance imaging (MRI) findings and concludes that they do not make sense. A clinical history may be incompatible with neurologic examination or test results. Examples of discrepancies abound. Red-flag symptoms missed in history-taking may include failure to inquire about fever, thunderclap-onset headache, intravenous drug abuse, empty medication bottles, or prolonged use of corticosteroids (Table 1.3). Essential to the history is documentation of medications the patient was taking or had recently (either deliberately or accidentally) discontinued. Some drugs are notoriously toxic, and others cause serious withdrawal symptoms; therefore, medication reconciliation is absolutely essential for a full history. Inaccurate history-taking leads to failure to order appropriate diagnostic imaging and missing the diagnosis.

Table 1.3

Urgent medication reconciliation

NOACs new oral anticoagulants, SSRIs selective serotonin reuptake inhibitors

And then there is a touchy issue. Although the young and less experienced are seldom bothered by the arrogance of their seniors, we are never absolved from making gross, regrettable errors through overconfidence. Arguably, errors should become less common as available knowledge increases—but not always. Even a seasoned, highly active, involved physician may be fooled by a slightly different presentation. Much of medical practice is pattern recognition, and knowing the patterns is critical to avoiding errors. However, clinical experience does not always reduce error rate; physicians can easily repeat the same mistake time and again. The most common bias is the so-called representativeness restraint. Physicians may miss important signs or try to force everything into a more recognizable scenario. History-taking is subject to confirmation bias, which reflects the tendency to discard contradictory data, to seek out data to confirm one’s preconceived idea, and to jump quickly to a diagnosis [3]. Confirmation bias does not allow for consideration of other possibilities and may lead to anchoring, when a history is cemented too early. Conditions that may seem acute may become chronic and vice versa after more information becomes available. While it is often useful to avoid getting distracted by incongruities, an important observation may occasionally require explanation. Errors are often in judgment and not exclusively procedural [4].

Hearing the Story: First Thoughts

We all think of something when we hear a story and often make provisional diagnoses after introductory comments. Thunderclap headache must be a ruptured aneurysm; ascending weakness after a period of tingling and upper respiratory infection must be Guillain–Barré syndrome; and headache, fever, and drowsiness must be a central nervous system (CNS) infection. Our thinking processes are causal simplicity and unremarkable ordinary. [5] Since medical school, we have been familiar with the saying, when you hear hoof beats, think horses, not zebras. Most physicians are taught to focus on the likeliest possibilities when making a diagnosis, not the unusual ones. Medicine is rife with red herrings. But often the easy explanation just fits perfectly, and it feels good to be certain. Over time and after many years of experience, this satisfying feeling will disappear, and our minds will constantly play the Devil’s advocate. We become less certain. We know that cookbook medicine does not exist. We know we do not like to be guided by the power of great anecdotes (the last-remembered case phenomenon). Be prepared that sometimes we will never know no matter how much we imagine. We must continue to doubt what we see and take nothing for granted.

When do we think there is an acute neuroemergency, and what are the early clues in the medical history? Here are my ten essential clues. These are (1) any new confusion, disorientation, or new, uncontrolled agitation; (2) acute decline in consciousness from sopor to stupor to coma; (3) any neuromuscular respiratory failure; (4) any acute new involuntary movement; (5) any acute new, persistent or progressing headache; (6) any obvious provoked or spontaneous asymmetry in movement; (7) any sensory sign over a large part of the body; (8) any motor sign that is progressing; (9) any acute inability to stand or walk; and (10) any new speech or language problem. Still, as we work diagnostically through known patterns and potential red flags (Table 1.4), we may decide the whole picture is out of context or aberrant. Often, unusual presentations of diseases require unusual inquiries, and these may come later when neuroimaging or laboratory tests are known. But causes often depend on the context. Coma in some emergency departments (EDs) is often attributable to a drug overdose.

Table 1.4

Red flags in history-taking

Construct a Clinical Trajectory

In the ICU, all is acute or urgent, but the commonly used adjectives (e.g., acute, hyperacute, subacute, and rapidly progressive) likely have different meanings for different people. However, it is useful to view illness in definable events such as time of onset, time to nadir, time in nadir or time with stable deficit, and rate of recovery. Certain neurocritical disorders have predictable clinical trajectory patterns. Before the recently acquired luxury of detailed neuroimaging, neurologists predicted a diagnosis on the clinical trajectory and findings on examination. Many of us still try to practice a priori estimations, and neuroradiologists also use these when interpreting images and estimating a posteriori probabilities.

A history can be more specific when the diagnosis is quickly established. Key questions are shown in Table 1.5. Moreover, a good history can provide a clinical trajectory; several examples are shown in Fig. 1.1. Acute occlusions of the middle cerebral artery often suddenly present with a major deficit—but not always. These patients present with a flaccid hemiparesis, forced eye deviation, and muteness of severe dysarthria (left hemisphere), and hemi-body neglect (right hemisphere). A well-known clinical scenario is a patient found after being missing for days, markedly dehydrated, and having severe rhabdomyolysis from pressure-induced muscle necrosis, all unfortunately because the patient was helpless and his situation unknown. Some patients improve substantially only to worsen when the collateral circulation fails [6–8]. The dilemma of whether clot removal will result in marked improvement or cause a worsened deficit (if the clot should break) remains unresolved. Occluded vertebrobasilar arteries often fluctuate markedly in posterior-circulation signs such as ataxia, dysphagia, and dysarthria [9–11].

Table 1.5

Key inquiries with major neurocritical illness

CPR cardiopulmonary resuscitation, OCP oral contraceptive pills, ACA anterior cerebral artery, MCA middle cerebral artery, VZV Varicella zoster virus, HSE herpes simplex encephalitis, NMDAR N-methyl D-aspartate receptor

Fig. 1.1

Clinical trajectories for common neurocritical disorders in the first hours/days (not including recovery trajectories)

There are two categories of patients who present with acute basilar artery occlusion [12, 13]. One has a rapid onset with nearly all deficits at presentation and is often found comatose with terminal breathing and posturing. Rhythmical jerking movements may occur unexpectedly and usually last 5 seconds. A common mistake is to regard this presentation as a seizure. The patient may be misdiagnosed as a postictal state, certainly if the brainstem is not sufficiently examined. Embolus to the basilar artery may also present with a locked-in syndrome (an awake state with minimal or no ability to respond to the examiner).

The second category of basilar artery occlusion presents with early warnings often related to a clot in the vertebral artery causing a stroke in the cerebellum. These patients start with acute severe vertigo and vomiting; only a careful neurologic examination will bring on a nystagmus, dysmetria, and inability to stand and walk but no weakness. Involvement of the distal (tip) basilar artery, where the superior cerebellar artery and posterior cerebral arteries branch off, may cause ischemia of the mesencephalon, thalami, inferior temporal lobes, and occipital lobes, which may cause signs and symptoms of acute diplopia, unstable gait, reduced or fluctuating consciousness, with moments of vigilance alternating with stupor. These patients develop a rostral brainstem infarction, a syndrome characterized by visual field defects, disorders of vertical gaze, convergence, a skew deviation, and pupillary abnormalities mostly resulting in small and poorly reactive pupils. Behavior abnormalities, including hallucinosis, are common. Visual field defects, including visual perseverations and scintillations in an optic field, have also been described. Many occipital infarcts are bilateral, and cortical blindness may be noted. Although a clot can dissolve and fully resolve [14–16], it is better to retrieve it while there are residual symptoms; clinical history has taught us to anticipate worsening later. Major improvement of clinical signs may not be fully reassuring and becomes important in decisions on endovascular treatment in acute stroke.

Patients with an aneurysmal subarachnoid hemorrhage often appear stable initially, looking (and feeling) great except for headache, but then acutely or gradually decline into a much worse neurological state. Rebleeding and acute hydrocephalus can pose major risks to the patient on the first day after aneurysmal rupture. Often, it is hard to overlook a rebleeding because the clinical changes are dramatic. Rebleeding may have occurred just before transport or even with transport. The seemingly well-looking patient may suddenly become stuporous or comatose, and new severe hypertension, tachypnea (or apnea), and tachycardia (or brief asystole) may accompany the altered consciousness. Motor responses change, and extensor posturing may occur [17–19]. The clinical trajectory of cerebral hemorrhage often involves more gradual symptoms than ischemic stroke. Small arterial bleeds lead to growing volume under pressure, damaging other arteries when they spread into the perivascular spaces, and tearing penetrating arteries or veins along the way. This domino effect progresses until platelet plugs appear surrounded by walls of red blood cells and fibrin – Fisher’s fibrin globes [20]. (A recent hyperacute hemorrhage in the CT scanner fully supports this concept [21].) This pathophysiology has a clear clinical correlate. Although hemorrhages can be suddenly catastrophic (and lethal), neurologic deficits typically appear more gradually, with worsening weakness and new deficits over several hours. Some patients experience a further decline in consciousness and an abrupt change in breathing (from early mass effect and brain-tissue shift). This gradual course is more common in putaminal and thalamic hemorrhages than in cerebellar hemorrhages because the compartments are larger and more accepting of newly increased volume. Not all hemorrhages are arterial; some are venous, classifying more as hemorrhagic infarcts. The majority of patients with a cerebral venous sinus thrombosis present with a gradual onset of headache, a localizing deficit (weakness, aphasia, or visual field cut), focal seizures, or all of the above. We need to ask many questions including a personal or family history of thrombophilia, contraceptive use, recent childbirth, ongoing or recent infections (e.g., otitis media, sinusitis, or mastoiditis), systemic inflammatory disease, malignancy (acute leukemia), recent traumatic brain injury (often minor and trivial), or excessive dehydration caused by combined vomiting and diarrhea [22].

The vast majority of patients with severe traumatic brain injury (TBI) have clinical symptoms of diffuse axonal brain injury. Depending on the impact and the damage to brain parenchyma, patients may be alert and able to follow commands, or they may be combative, agitated, or comatose with abnormal motor responses [23, 24]. The clinical trajectory is determined by worsening hemorrhagic contusions, massive malignant cerebral edema, or further extension of an extra-axial hematoma. Extracranial blood, present either in the subdural or epidural compartment, can also determine the course in traumatic brain injury. The lucid interval after trauma may be indicative of epidural hemorrhages, but blossoming contusions may be more common than has been truly appreciated.TBI commonly correlates with alcohol intoxication or drug use, thus easily confounding and masking the typical trajectory. High blood-alcohol levels correlate with an increased expansion rate [25]. Patients with TBI may have clinical deterioration from a systemic complication. The risk of early acute respiratory distress syndrome (ARDS) is high. Disseminated coagulopathy can be anticipated with penetrating gunshot wounds and change the presentation and trajectory dramatically.

The two most common acute neuromuscular disorders in the Neuro Intensive Care Unit are Guillain–Barré syndrome (GBS) and myasthenia gravis, but they have markedly different presentations. GBS proceeds in a stepwise fashion, using several days to reach a nadir. Myasthenia gravis, however, may fluctuate from a near-normal examination to marked weakness within the same day. Recognizing fatigable weakness often clinches the diagnosis. Myasthenia gravis patients often have abnormal eye movements, oropharyngeal weakness, and proximal limb weakness. Bulbar function must be specifically queried and examined, as it may determine the need for elective intubation. Myasthenia gravis-based muscle weakness occurs in the masseters, and jaw opening is typically stronger than jaw closure. Progressive neuromuscular transmission failure in the diaphragmatic muscle may occur in 30% of patients with myasthenia gravis at the time of diagnosis. One cause of in-hospital deterioration in myasthenia gravis is significant worsening within the first days of corticosteroid administration. Often, this clinical worsening is observed in patients exposed to corticosteroids for the first time, but it also can occur when the initial doses are high. When we see these patients for the first time, we can expect to see them visibly struggling to breathe or to sit up in bed, maintaining only marginal pulse-oximeter values, despite increasing oxygen requirements. When answering questions, patients appear unable to catch their breath or to resume normal breathing following the simplest exercise. Myasthenic crisis may also involve a serious overdose of cholinergic drugs with sweaty, salivating patients complaining of abdominal cramps and vomiting (in medical parlance, SLUDGE –salivation, lacrimation, urination, defecation, gastrointestinal upset, and emesis).

Traumatic spinal cord injury is acute and complete, although symptoms may improve when the spinal shock phase resolves [26]. Spinal cord infarct is also acute but may initially be gradual before a very sudden loss of motor function, which occurs up to 12 hours after initial onset [27].

CNS infections usually progress gradually, albeit more quickly in acute bacterial meningitis. Nevertheless, patients appearing mildly lethargic or obtunded on initial presentation may become deeply comatose within hours.

After the acute phase, a number of events determine the clinical course in patients with acute brain injury. First, obstructed CSF flow causes further deterioration unrelated to the primary event. Examples include aneurysmal subarachnoid hemorrhage, thalamic ventricle-trapping hemorrhages, cerebellar hematomas obliterating the fourth ventricle, or simply hemorrhage breakthrough into the ventricular system blocking outflow. Second, expansion due to cerebral edema and often driven by increased intracranial pressure can threaten the airway until patients need intubation. A neurosurgical intervention, such as evacuation of a hematoma or ventriculostomy placement, often interrupts a downward spiral in the clinical course. Later clinical trajectories are often determined by the aggressiveness of interventions and not by the natural history alone.

These specific clinical trajectories can often be obtained after a careful history and significantly add to a full description of the clinical picture. It is anticipatory information for attending neurointensivists – forewarned is forearmed.

More Reflections

Cabot and Adams wrote in 1938: The history is the key to diagnosis .... More errors in diagnosis are traceable to lack of acumen in eliciting or interpreting symptoms than have ever been caused by a failure to hear a murmur, feel a mass, or take an electrocardiogram. [28] It has been known for centuries that a patient history is more than the patient’s story and must also include the physician’s interpretation [29]. The names patients give to their prior illnesses may be incorrect. Physicians are often required to correct self-diagnoses offered by the patient. The patient history is therefore a construct and not just an expression of the patient’s narrative. The final physician history is a careful organization of true facts. The art of history-taking requires knowledge of disease and considerable experience to steer patients and families in the right direction. Test results are often emphasized by the person who provides the history, but physicians are concerned with symptoms. Physical examination cannot be only real path to diagnosis. Taking a clinical history takes time, which is not always available. Cell phones or pagers predictably interrupt the encounter and preclude careful listening. Physicians often redirect opening statements of patients and families but also direct questions toward a specific concern; we have no patience and redirect already after 20 seconds on average [30, 31]. Failures of information-gathering and integration are due to the provider feeling pressed for time. We must close out distractions and force the mind to slow down. Most errors are related to process breakdowns in the patient–practitioner clinical encounter. Diagnostic errors can be traced to cognitive errors by physicians, particularly in synthesizing the available information to identify the correct diagnosis. We may be saved by modern neuroimaging, which greatly increases the diagnosis of neurologic disorders, but diagnostic errors have far from disappeared. Better neuroimaging does not replace the need for systematic diagnostic reasoning, also because correct interpretation of brain imaging is very difficult and relies on both detailed clinical information and communication with the neuroradiologist.

Complacency is difficult to address, and I understand why. Physicians tend to generate a working diagnosis almost immediately upon hearing a patient’s initial symptom presentation and want to seek a familiar pattern without exploration of other possibilities. Mostly, the diagnosis is correct, appropriate tests are ordered, and effective treatment begins. This pattern is common, difficult to change, and, counterintuitively, reassuring to families. However, exceptions must always be considered. According to Berner and Graber, physicians acknowledge the existence of diagnostic error but think the likelihood is less than it really is [32]. Vickrey advises deliberate pursuit of another angle: Let’s play devil’s advocate or Let’s re-review elements of the history. [3]

Deliberately considering a differential diagnosis prior to the final decision is essential to diagnostic reasoning. The most common breakdown points are test ordering and interpretation, performance of the medical history and physical examination, and initiation of consultations. While praising independence, we should also, once in a while, seek opinions from colleagues. Failure to order appropriate tests is the most frequent breakdown.

Getting the history right is a core principle. A phone call to family members or direct communication is essential to acquire a sense of the time course and urgency. Seemingly acute conditions may actually be chronic and vice versa as more information becomes available. Clinical presentations unique to neurointensive care include the comatose patient found down, rapidly progressive weakness, respiratory failure without obvious pulmonary or cardiac triggers, and, inevitably, the mysterious, progressive encephalopathy with abnormal CSF and hard-to-pinpoint MRI abnormalities. Often, with hindsight and a better history, the clinical diagnosis becomes obvious. None of us will forget the CSF we should have requested to diagnose meningitis had we but known of the looming infection and fever. If we had queried another patient about his unremitting back pain before he lapsed into unresponsive septic shock, we might have ordered an MRI of the spine to diagnose an epidural abscess. Painful, acute double vision indicates an urgent need for vascular studies and contrast-enhanced MRI to demonstrate a growing and unstable cerebral aneurysm. We expect cerebral vasospasm to follow a ruptured aneurysm, but it may come earlier than anticipated if we are unaware that the presenting headache was already a rebleed. Unexplained respiratory failure becomes clearly neurologic when the history reveals progressive dysphagia, muscle-mass loss and twitching (motor neuron disease), diplopia, and weakness increasing with exercise or repetitive use but with day-to-day variation, yet typically strong after a good night’s rest (myasthenia gravis). I have seen a basilar artery embolus present as coma following a pulseless electrical activity arrest; only after the spouse arrived did a story of acute dysphagia, vertigo, and alternating weakness emerge to suggest that respiratory arrest preceded the cardiac arrest.

In the new era of intensive-care imaging with handheld and smartphone-connected devices, the clinical history may be sidelined even more. Who wants to know what really happened if we can see it already? Are examination and imaging not enough? Without diminishing these parts of the clinical assessment, we should approach them cautiously, with the intent to achieve accuracy. If pressed for time, it may be preferable to tailor the examination and spend more time taking a history. Information-gathering starts within the first moments of an encounter. Do not assume anything; verify everything. Generalization is not enough and we need to delve deeper if we can. We should warn against quick conclusions such as what follows a sign (post hoc) and therefore is caused by it (ergo propter hoc). Biases in taking history are prevalent, but hopefully we avoid them. (Table 1.6).

Table 1.6

Biases in taking a history

Pointers and Takeaways

Of course, taking a history and guiding the conversation remain the most critical skills of a neurointensivist, but don’t assume they are acquired easily. Important information comes to those who keep asking.

Urgency is not appreciated enough and should be established.

Particularization of a clinical problem is needed for a rational decision, even in emergency settings. Be aware of the fallacy of generalization.

Precipitating factors may provide important clues to unresolved cases.

Clinical trajectories have been observed for most neurocritical illnesses and provide foresight into what may come next.

References

1.

Gandhi TK. Fumbled handoffs: one dropped ball after another. Ann Intern Med. 2005;142:352–8.Crossref

2.

Riesenberg LA, Leitzsch J, Massucci JL, et al. Residents’ and attending physicians’ handoffs: a systematic review of the literature. Acad Med. 2009;84:1775–87.Crossref

3.

Vickrey BG, Samuels MA, Ropper AH. How neurologists think: a cognitive psychology perspective on missed diagnoses. Ann Neurol. 2010;67:425–33.Crossref

4.

Rolston JD, Bernstein M. Errors in neurosurgery. Neurosurg Clin N Am. 2015;26:149–55. viiCrossref

5.

Montgomery K. How doctors think: clinical judgment and the practice of medicine. Illustrated ed. New York: Oxford University Press; 2005.

6.

Antunes Dias F, Castro-Afonso LH, Zanon Zotin MC, et al. Collateral scores and outcomes after endovascular treatment for basilar artery occlusion. Cerebrovasc Dis. 2019;47:285–90.Crossref

7.

Hernandez-Perez M, Perez de la Ossa N, Aleu A, et al. Natural history of acute stroke due to occlusion of the middle cerebral artery and intracranial internal carotid artery. J Neuroimaging. 2014;24:354–8.Crossref

8.

Huttner HB, Schwab S. Malignant middle cerebral artery infarction: clinical characteristics, treatment strategies, and future perspectives. Lancet Neurol. 2009;8:949–58.Crossref

9.

Conforto AB, de Freitas GR, Schonewille WJ, Kappelle LJ, Algra A, Group BS. Prodromal transient ischemic attack or minor stroke and outcome in basilar artery