The neurologic examination in clinical practice: Why, who and what should health care providers care to practice?

Ideally, patients seek medical advice from their established primary health care provider (HCP) who would, in turn, diagnose and treat their problems or, if necessary, send them to an acute care facility or refer them to a neurologist depending on the urgency of their condition. Approximately 10% of visits to primary care practices are due to neurological issues (Miller, 1986; Papapetropoulos, Tsibre, & Pelekoudas, 1989). Primary HCPs diagnose and treat common neurologic disorders; e.g. they cannot afford to defer treatment of patients with Bell’s palsy or temporal arteritis to a neurologist they will see in a couple of weeks or longer. Diagnosis must be made or suspected promptly and steroid treatment must be started shortly after onset of symptoms to have best chances of recovery in the former and prevent blindness in the latter. In neither case, will neuroimaging, a heavily overused or abused diagnostic tool, provide appropriate answers. On the contrary, neuroimaging in these cases may be falsely reassuring, delay treatment and waste money and resources. Thus, mastery of procedural and analytical skills of the neurological method is a must for primary HCPs, especially in countries where health systems are underdeveloped or developing and neurological services are not sufficient.

So we have primary HCPs who can take care of our patients’ neurological problems, right? Well, not quite. On behalf of the American Academy of Neurology (AAN), American Neurology Association and Association of Neurology Professors in Neurology the AAN wrote to the Association of American Medical Colleges (AAMC) and the American Medical Association (AMA) in 2009 appealing for inclusion of a clinical experience in neurology as a requirement of the medical school curriculum (personal communication). The AAN argues that nearly 20% of hospital inpatients are admitted due to a primary neurological problem, and the proportion with secondary neurological diagnosis is much higher (Menken, 1986; Playford, Crawford, & Monro, 1994). At that time, stroke and Alzheimer’s dementia ranked as the third and seventh leading causes of death, respectively, in the U.S. The AAN further deliberates that most patients with neurological problems such as stroke will not be seen or evaluated by neurologists hence neurological training for future non-neurologists is crucial (Brown, Lisabeth, Garcia, Smith, & Morgenstern, 2004).

The insufficiency of core neurological skills training in medical school and beyond is likely a major contributor to the high rates of misdiagnosis of neurologic emergencies by frontline HCPs. For example, nearly 10% of stroke patients and 20% of awake subarachnoid hemorrhage patients are missed at first medical contact with a primary care or emergency physician, frequently with devastating outcomes (Kowalski et al., 2004; Newman-Toker & Pronovost, 2009). In this day and age there has been excessive dependence on neuroimaging for diagnosis of patients’ ailments. Advanced technology has in some part made us complacent and reduced our efforts in making a prioritized differential diagnosis based on history and the physical examination. Physicians are trained to do the best they can to relieve suffering of their patients and make them feel better. At least physicians should do no harm to their patients. A head CT or MRI may be completely negative or may show incidental findings that have none or little to do with the chief complaint of our patients. Even worse, a patient will gain nothing but complications or side effects of a procedure performed for the incidental finding detected on CT or MRI, leaving problems the patient sought medical attention for undiagnosed and sometimes untreated.

An example in point is a 48 year-old lady that presents with episodes of left hand numbness and an MRI of the head reveals a meningioma over the right frontal convexity. Clearly, in this case, good history taking and review of systems will result in a few prioritized possibilities including ischemic heart disease, focal nerve compression (carpal tunnel syndrome or ulnar neuropathy depending on the distribution of numbness), radiculopathy due to nerve root compression (like in a protruding disc disease), a cortical lesion in the right parietal lobe, or even psychosomatic disease; all have nothing to do with the incidental meningioma in the frontal lobe. Knowing the basics of neuroanatomy will direct the physician to look for certain signs that may support suspected diagnoses in this case; namely, distribution of numbness and hypoesthesia, Tinel’s sign, Phalen’s sign, asymmetric hyporeflexia, agraphesthesia, astereognosis, asymmetric two-point discrimination, asymmetric opto-kinetic nystagmus, hemi-neglect or ideomotor apraxia. Naturally, one can argue that the latter five signs may require expertise of a neurologist or a behavioral neurologist; however, we can agree that a primary HCP or any non-neurologist HCP should be familiar with the former four.

This raises the question of what essentials of the NE should non-neurologist primary or other HCPs know and practice? In a survey of six texts and the AAN clerkship core curriculum (Gelb, Gunderson, Henry, Kirshner, & Jozefowicz, 2002), Moore et al. find 94 different elements of the NE (Moore & Chalk, 2009). They argue that while no studies identifying the essential elements of the NE exist, experienced neurologists perform an adequate NE in a few minutes and examples of a screening NE have been published (Gelb et al., 2002).

Now that we agree the NE is important in our practice, how do we deal with the anxiety of neurophobia (Flanagan, Walsh, & Tubridy, 2007). The answer is simple; get to know the essentials of the NE. Humans fear the unknown and are at ease with things they know. If you learned it before, relearn it. You may feel you’ve forgotten all the neuroscience you learned, but you will be surprised by how quickly you can relearn it (AAN website 2012). If you have never had structured teaching in neurology (you are not alone; many medical schools do not have a required neurology clerkship), reach out to your colleagues and grab every opportunity to increase your exposure to patients with neurological problems and increase your bedside neurology “mini-tutorials”. After all this is the spirit of continued professional development (CPD) and all of us, HCPs, continue to learn throughout our careers.

The essentials of the NE include mental status, cranial nerves, motor function (including gait and coordination), reflexes (including Babinski) and sensation. It is important to perform the exam in that order to reduce the chances of forgetting any element. As the first step in diagnosing neurological disease is to localize the lesion, it is important to study and remember the few major system pathways and where they run. Learn how to recognize lower motor neuron (LMN) vs. upper motor neuron (UMN), descending (e.g. corticospinal) vs. ascending (e.g. spinothalamic, dorsal column large sensory fibers) tracts, presentations of muscle weakness (e.g. focal or lateral vs. generalized or diffuse, fatigable vs. constant, proximal vs. distal), functions of the cranial nerves, and a few common stroke territories and syndromes. The neurology clerkship curriculum (Gelb et al., 2002) includes examples of components that should be covered in a NE depending on the clinical presentation of the patient. Appendices I-III summarize guidelines for a comprehensive NE, a screening NE and NE in patients with altered level of consciousness, respectively.

Clearly, certain situations may call for other detailed testing. For example, eliciting primitive reflexes (palmar grasp, suck, glabellar, snout, and routing), impaired word fluency (Thurston word fluency test), echopraxia, and go-no-go test in a patient with dementia and frontal lobe dysfunction. In another situation, looking for a sensory level and checking rectal tone and perianal sensation would be part of a focused NE in a patient with acute/subacute back pain, lower extremity weakness/numbness with or without bowel/bladder incontinence. A third situation would be checking for a relative afferent pupillary defect in a patient with suspected optic neuritis. One more situation would be minimizing ambient lighting to enhance pupillary asymmetry and confirm the meiotic eye (rather than mydriatic eye) as the abnormality in a patient with suspected Horner’s syndrome, which can be the first sign in a patient with a pancoast tumor.

Tools necessary to perform a thorough NE include: reflex hammer, tuning fork (128 Hz for testing vibration; a 1000 Hz tuning fork is a plus for Rinne/Weber test), eye chart, penlight (fresh batteries for bright light), sensory kits (e.g. tongue depressors, cotton swabs, monofilament, single-use pins) and your two free hands. A stethoscope is important to check for carotid, ophthalmic and other bruits and an ophthalmoscope is important for detecting optic atrophy (pallor of the optic disc), subarachnoid hemorrhage, retinal disease, increased intracranial pressure (papilledema) and glaucoma (large cup/disc ratio). A red card or object may help in eliciting red desaturation in patients with suspected optic neuritis or multiple sclerosis.

Finally, patience, common sense, practice and systematic approach will generally desensitize any phobias and, in my opinion, minimize neurophobia, which many HCPs have. Consider reviewing the components of the NE, asking your neurologist to call you when s/he is performing a NE on your patients, and performing a full NE on every patient, when possible, to establish comfort and become confident and proficient in assessing normalcy and calling abnormalities. Look for the big picture and do not fall prey for intricacies and details of the NE. Search for focal abnormalities, asymmetries, and distribution of weakness/numbness (ask if distal more or less than proximal or upper more or less than lower) in an attempt to localize the lesion; subsequently, you can prioritize your differential diagnosis and focus your work up to investigations of higher yield. With practice, you should feel confident in your NE techniques and call it areflexia when you cannot elicit patellar reflexes (rather than “I could not get reflexes on my examination”). In a young adult presenting with subacute ascending weakness areflexia should lead you to suspect a diagnosis of acute inflammatory demyelinating polyradiculopathy (a.k.a. Guillian Barre Syndrome), a potential emergency requiring appropriate monitoring and care.

With perfect practice you can diagnose a right visual field deficit in less than 15 seconds and avoid unnecessary work up looking for right hemi-body bruises in a man accused of harassment bumping into people walking by, door knobs, tables and walls. With systematic practice you will develop a habit to assess for response to auditory, visual and noxious stimuli and perform special cranial nerve testing (see under examination in a patient with altered mental status above) in an “unresponsive” patient. In these situations you will be able to suspect encephalopathy, brain death, or psychogenic coma or may discover that your “unresponsive” patient is fully awake and responsive, like the case of a consult I see on the surgical wards during residency 30 years ago. On postsurgical rounds one day in the early morning, patient reportedly does not respond to sound and visual stimuli and neurology consult is requested. On examination the patient has severe bilateral hearing loss, binocular blindness with preserved response to visual threat, and prompt and appropriately startled response to a brisk rub of his legs. He turns out to have pre-existing severe hearing loss and a recent bilateral occipital stroke presenting as Anton’s syndrome (cortical blindness and visual confabulation) without impairment of alertness. At the end, it pays to be systematic and touching the patient, a next step after failure to elicit responses to auditory or visual stimuli, yields normal alertness and saves the day, for me, in that case 30 years ago, and in every case I see.

Appendix I

In a patient with neurological disease a comprehensive NE should include the following components:

Level of alertness, orientation in four spheres (person, place, time and insight to one’s illness), language (fluency, repetition, comprehension and naming), thought and speech (e.g. slurred, stuttering, pressured, superficial), memory (short-term and long-term), calculation, visuo-spatial processing (drawing a clock, locating places on a map, intersecting pentagons) and abstract reasoning. The mini-mental status examination can serve as a graded test of HCFs useful in initial evaluation and later follow up of patients with progressive dementing illnesses such as Alzheimer’s disease.

Cranial nerves

  • Vision (visual fields, visual acuity, and fundoscopic examination)
  • Pupillary light reflex
  • Facial sensation
  • Facial strength (muscles of facial expression)
  • Hearing
  • Palatal movement
  • Speech
  • Neck movements (head rotation, shoulder elevation)
  • Tongue movement

Motor function

  • Gait (casual, on toes, on heels, and tandem gait)
  • Coordination (rapid alternating movements, finger-to-nose, and heel-to-shin)
  • Involuntary movements
  • Pronator drift
  • Tone (resistance to passive manipulation)
  • Bulk
  • Strength (shoulder abduction, elbow flexion/extension, wrist flexion/extension, finger flexion/extension/abduction, hip flexion/extension, ankle dorsiflexion/plantar flexion)


  • Deep tendon reflexes (biceps, triceps, brachioradialis, patellar, Achilles)
  • Plantar responses


  • Light touch
  • Pain or temperature
  • Proprioception
  • Vibration
Appendix II

In a patient with no neurological symptoms a screening NE should include at least some assessment of each of the five major components of the comprehensive NE.

Naturally, if you suspect neurologic disease based on the patient’s history or your findings on the
screening NE, a more complete NE may be necessary. Conversely, specific signs should be looked for in
a focused examination when a particular diagnosis is suspected (e.g. Tinel’s and Phalen’s signs in a patient with suspected carpal tunnel syndrome). An example of a screening NE would include the following:

Mental status (level of alertness, appropriateness of responses, orientation to date and place)

Cranial nerves

  • Visual activity
  • Pupillary light reflex
  • Eye movements
  • Hearing
  • Facial strength (smile, eye closure)

Motor function

  • Gait (casual, tandem)
  • Coordination (fine finger movements, finger-to-nose)
  • Strength (shoulder abduction, elbow extension, wrist extension, finger abduction, hip flexion, knee flexion, ankle dorsiflexion)


  • Deep tendon reflexes (biceps, patellar, Achilles)
  • Plantar responses


(one modality at toes; can be light touch, pain/temperature, or proprioception)

Appendix III

In a patient with altered level of consciousness the NE should include:

Mental status

  • Level of arousal
  • Response to auditory stimuli (including voice)
  • Response to visual stimuli
  • Response to noxious stimuli (applied to the midline and each limb individually)

Cranial nerves

  • Response to visual threat
  • Pupillary light reflex
  • Oculo-cephalic (doll’s eyes) reflex
  • Vestibulo-ocular (cold caloric) reflex
  • Corneal reflex
  • Gag reflex

Motor function

  • Voluntary movements
  • Reflex withdrawal
  • Spontaneous, involuntary movements
  • Tone


  • Deep tendon reflexes
  • Plantar


(to touch or pressure first then to noxious stimuli)


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Written by
Basim M. Uthman, MD, FACP, FAAN
Professor & Vice Chair, Clinical Neurology,
Professor of Clinical Neuroscience,
Director Neurology Clerkship
Weill Cornell Medical College in Qatar,
Doha, Qatar