Neurological History And Examination
Introduction
These notes may be of interest to anyone who works in the area of clinical neurology. We start with some basic outlines for history and examination followed by a small discussion on the role of tests in the workup of any condition.
(1) Introductions.
- Introduce yourself and your team.
- Ask if visitors are family or friends (do not assume anything).
(2) Background.
- Ask where the patient is from.
- Ask how they keep themselves busy (work, study, unemployed).
(3) History of Presenting Complaint.
- Open history first; let the patient talk (try not to interrupt and only speak up if something needs to be clarified).
- Closed questions later; try to be orderly (if you do not know the diagnosis, make a problem list and assess each problem in turn; if you think you know the diagnosis, assess risk factors, make a differential list, and assess risk factors for each differential in turn).
(4) Past Medical History.
- Focus on the relevant aspects.
(5) Social History.
- Ask about sleep, chronic stress, and depression.
- Ask about smoking, alcohol, and illicit drugs.
(6) Family History.
- This may or may not be relevant.
(7) Medications.
- If you have a list, ask whether it is current.
- Ask about adherence and side-effects.
(8) Allergies.
- Do not ever forget this; ask about allergies every single time.
(1) Introductions.
- Introduce yourself and your team.
- Ask if visitors are family or friends (do not assume anything).
(2) Background.
- Ask where the patient is from.
- Ask how they keep themselves busy (work, study, unemployed).
(3) History of Presenting Complaint.
- Open history first; let the patient talk (try not to interrupt and only speak up if something needs to be clarified).
- Closed questions later; try to be orderly (if you do not know the diagnosis, make a problem list and assess each problem in turn; if you think you know the diagnosis, assess risk factors, make a differential list, and assess risk factors for each differential in turn).
(4) Past Medical History.
- Focus on the relevant aspects.
(5) Social History.
- Ask about sleep, chronic stress, and depression.
- Ask about smoking, alcohol, and illicit drugs.
(6) Family History.
- This may or may not be relevant.
(7) Medications.
- If you have a list, ask whether it is current.
- Ask about adherence and side-effects.
(8) Allergies.
- Do not ever forget this; ask about allergies every single time.
Neurological Examination
The neurological examination should never be rushed, although it often tempting to do so. However, it can be divided into sections, and it is reasonable to employ only those sections that are relevant to the symptoms of the current patient.
(1) General.
(1) General.
Bedside view
Brief cardiac examination |
Pause and have a look - are they sick or not.
Inspect hands. Palpate radial pulse. Auscultate carotids and heart. Record blood pressure. |
(2) Arousal and Attention.
GCS
Mental screen (ORAM) |
Eyes (spontaneously 4, to voice 3, to pain 2, nothing 1).
Voice (oriented 5, disoriented 4, inappropriate 3, incoherent 2, nothing 1). Motor (obeys commands 6, localizes to pain 5, withdraws to pain 4, decorticate 3, decerebrate 2, nothing 1). Orientation (day/month/year, department/city/country). Registration (apple, table, penny). Attention (serial sevens or WORLD backwards). Recall (apple, table, penny). |
(3) Speech.
Generation
Comprehension Repetition Articulation |
Fluency (describe a picture).
If necessary, check naming (parts of hand or shirt). Writing (sentence). Three-stage command (with your right hand touch your chin, then your nose, then your right ear). If necessary, check one-stage command (close your eyes). Sentence (say no ifs, ands, or buts). Phrases (say city/citizen/citizenship, baby hippopotamus, red leather yellow leather). |
(4) Cranial Nerves.
1
2, 3, 4, 6 (IAFFPE) 5
7 8 9, 10 11 12 |
Face sensation (light touch and pinprick).
Jaw strength. Close eyes and show teeth. Sugar on tip of tongue. Acuity (crude testing by rubbing fingers, fine testing at 256/512 Hz via Weber's and Rinne's - go to louder ear). Dix-Hallpike (both sides, head over table edge at 45 degrees, check for nystagmus and vertigo). Say ah (look for full and symmetric elevation of palate). Say ka (dysarthria). Gag reflex (bilaterally). Shrug shoulders. Rotate head to side. Stick tongue out and move side to side. |
(5) Upper Limbs.
Inspection
Tone Power (0-5) Reflexes Coordination Sensation |
Check for wasting and fasciculations.
Look at the back - if winging, assess trapezius (shoulder abduction) and serratus anterior (shoulder flexion). Check elbow and wrist tone. Assess for downward and pronator drift (arms extended, palms up) for ten seconds. Roots - C5 (deltoid), C6 (brachioradialis), C7 (triceps), C8 (FCU), T1 (interossei). Nerves - median (FPL, APB, FDP1), ulnar (FDP4, interossei), radial (EDC, EIP). Biceps brachii (C5/6), brachioradialis (C6), and triceps (C7). Finger to nose (past-pointing, intention tremor) and follow the finger (overshoot). Begin distally and if sensory loss is detected in a particular area proceed outward to determine boundaries - assess light touch (both spinal tracts), pinprick (spinothalamic tracts), and proprioception (dorsal columns). |
(6) Lower Limbs.
Inspection
Tone Power (0-5) Reflexes Coordination Sensation |
Check for wasting and fasciculations.
Check knee tone and for ankle clonus (sustained clonus of more than 3-4 beats is always abnormal). Assess drift for ten seconds. Roots - L2 (iliopsoas), L3 (quadriceps), L4 (TA), L5 (extensor hallucis longus), S1 (gastrocnemius). Nerves - femoral (iliopsoas), inferior gluteal (TFL), sciatic (hamstrings), peroneal (TA), tibial (gastrocnemius). Quadriceps (L3/4), Achilles (S1), and plantars. Heel to shin. Assess light touch, pinprick, and proprioception. |
(7) Gait.
Walking
Stand with feet together Heel-toe Romberg's Stand on toes and heels Squat |
Cerebellar ataxia (poor balance, wide base, may stagger or reel).
Sensory ataxia (poor balance, wide base, stomping, may watch feet). Hemiplegic/Circumducting (upper limb flexed, lower limb extended, both internally rotated). Paraplegic/Scissors (crouching with hips and knees flexed and both lower limbs circumducting). Parkinsonian (slow start, reduced arm swing, festination - small shuffling steps and forward flexed posture). Marche a petit pas (upright body, slow start, small shuffling steps, wide base, and preserved arm swing). Myopathic/Dystrophic (waddling with pelvis tilted down on unsupported side). Neuropathic/Steppage (cannot dorsiflex foot). Spastic (stiff, foot-dragging walk). Antalgic (one foot is in contact with the ground for shorter duration than usual). Ataxia. Ataxia. Sensory ataxia. Distal weakness. Proximal weakness. |
Coma
There are various etiologies for coma (reduced arousal and awareness) and the differentials include brain death (no arousal or awareness), persistent vegetative state (arousal, no awareness; from hypoxia, ischemia, trauma, or stroke affecting the thalamus and cerebral hemispheres bilaterally), minimally conscious state (arousal, minimal but definite awareness), locked in syndrome (arousal and awareness; from damage to the pons), and psychogenic unresponsiveness (arousal and awareness).
(1) Coma etiology.
- Should be pursued to exclude a reversible etiology.
(a) Supratentorial structural coma.
- May be fixed and dilated (3rd nerve compression) or normal.
- May be a gaze preference towards the lesion side (away from hemiparesis).
- Localizing motor responses.
- Etiologies include subdural hematoma, epidural hematoma, intracerebral hemorrhage, stroke, brain tumour, cerebral contusion, and brain abscess.
(b) Subtentorial structural coma.
- May be fixed and midsized (midbrain damage), pinpoint (opioids, pons damage), or normal.
- May be a gaze preference away from the lesion side (towards the hemiparesis).
- Localizing motor responses.
- Etiologies include basilar artery thrombosis/top of the basilar embolic occlusion, pontine hemorrhage, cerebellar hemorrhage or infarction, and posterior fossa subdural and epidural hematomas.
(c) Metabolic coma.
- Typically, reactive pupils in the presence of otherwise impaired brainstem dysfunction (although they may be unreactive with opioids or anticholinergics).
- Normal eye movements (although they may be impaired by sedatives or Wernicke's encephalopathy).
- Symmetrical motor responses (although they may be asymmetric in postictal state, hypoglycemia, hyperosmolar hyperglycemia, or hepatic encephalopathy).
- Etiologies include most of those for acute confusion minus the structural etiologies (use the acronym SEIES).
(2) Diagnosis of brain death.
- In ANZ, the determination of brain death requires a clinical setting in which there is irreversible unresponsive coma, absence of brainstem reflexes, and absence of respiratory drive in the absence of sedatives, neuromuscular blockade, hypothermia, and shock. Metabolic coma differentials must be excluded and three criteria fulfilled.
(a) Unresponsive coma.
- GCS (GCS 3 - eyes closed, no voice response, no pain response to sternal or nailbed pressure; ignore the Lazarus sign).
(b) Absent brainstem reflexes.
- Pupil reflex (fixed pupils - may or may not be dilated).
- Corneal reflex (absent bilaterally).
- Occulocephalic reflex (check for neck injuries first, no response to horizontal and vertical doll's eye maneuvers - normally, the eyes should move in the direction opposite to head rotation).
- Oculovestibular reflex (do otoscopic examination to exclude tympanic rupture first, no response with 50 ml cold water injected into each ear - normally, in comatose patients with intact brainstem function the eyes deviate towards the irrigated side, and in awake patients there is additional nystagmus with the fast phase directed away from the irrigated side).
(c) Absent respiratory drive.
- Apnea test (disconnect ventilator and wait five minutes, if carbon dioxide levels rise above normal the test is failed).
Regarding prognosis, persistent myoclonus status indicates 99% chance of poor outcome, combined absent pupil and corneal reflexes indicates 99% chance of poor outcome, absent cortical potentials on somatosensory evoked potentials (SEPs) indicates 95% chance of poor outcome, and burst-suppression or flat EEG indicates 80% chance of poor outcome.
(1) Coma etiology.
- Should be pursued to exclude a reversible etiology.
(a) Supratentorial structural coma.
- May be fixed and dilated (3rd nerve compression) or normal.
- May be a gaze preference towards the lesion side (away from hemiparesis).
- Localizing motor responses.
- Etiologies include subdural hematoma, epidural hematoma, intracerebral hemorrhage, stroke, brain tumour, cerebral contusion, and brain abscess.
(b) Subtentorial structural coma.
- May be fixed and midsized (midbrain damage), pinpoint (opioids, pons damage), or normal.
- May be a gaze preference away from the lesion side (towards the hemiparesis).
- Localizing motor responses.
- Etiologies include basilar artery thrombosis/top of the basilar embolic occlusion, pontine hemorrhage, cerebellar hemorrhage or infarction, and posterior fossa subdural and epidural hematomas.
(c) Metabolic coma.
- Typically, reactive pupils in the presence of otherwise impaired brainstem dysfunction (although they may be unreactive with opioids or anticholinergics).
- Normal eye movements (although they may be impaired by sedatives or Wernicke's encephalopathy).
- Symmetrical motor responses (although they may be asymmetric in postictal state, hypoglycemia, hyperosmolar hyperglycemia, or hepatic encephalopathy).
- Etiologies include most of those for acute confusion minus the structural etiologies (use the acronym SEIES).
(2) Diagnosis of brain death.
- In ANZ, the determination of brain death requires a clinical setting in which there is irreversible unresponsive coma, absence of brainstem reflexes, and absence of respiratory drive in the absence of sedatives, neuromuscular blockade, hypothermia, and shock. Metabolic coma differentials must be excluded and three criteria fulfilled.
(a) Unresponsive coma.
- GCS (GCS 3 - eyes closed, no voice response, no pain response to sternal or nailbed pressure; ignore the Lazarus sign).
(b) Absent brainstem reflexes.
- Pupil reflex (fixed pupils - may or may not be dilated).
- Corneal reflex (absent bilaterally).
- Occulocephalic reflex (check for neck injuries first, no response to horizontal and vertical doll's eye maneuvers - normally, the eyes should move in the direction opposite to head rotation).
- Oculovestibular reflex (do otoscopic examination to exclude tympanic rupture first, no response with 50 ml cold water injected into each ear - normally, in comatose patients with intact brainstem function the eyes deviate towards the irrigated side, and in awake patients there is additional nystagmus with the fast phase directed away from the irrigated side).
(c) Absent respiratory drive.
- Apnea test (disconnect ventilator and wait five minutes, if carbon dioxide levels rise above normal the test is failed).
Regarding prognosis, persistent myoclonus status indicates 99% chance of poor outcome, combined absent pupil and corneal reflexes indicates 99% chance of poor outcome, absent cortical potentials on somatosensory evoked potentials (SEPs) indicates 95% chance of poor outcome, and burst-suppression or flat EEG indicates 80% chance of poor outcome.
Comparing Tests And Treatments
Ideally, one should be able to identify the diagnosis after a thorough history and examination. The additional workup using the arsenal of tests available at most hospitals should be used to confirm that diagnosis, and exclude differential diagnoses (in practice, however, tests are often used in a "shotgun" approach whenever one has little to no idea about what they are looking for - this is sometimes necessary, but not ideal). Moreover, a variety of treatments are often available for any one condition. In order to compare different tests with each other, and different treatments with each other, a few terms will be important to remember over the next few sections as shown below.
(1) Gold standard.
- The best available diagnostic test.
(2) Sensitivity.
- If a patient has a condition, the chance that the test will come back positive.
- If a 100% sensitive test is positive, the patient MAY have the condition but assuming sub-par specificity there will be some false positives.
- If a 100% sensitive test is negative, the patient DOES NOT have the condition.
(3) Specificity.
- If a patient does not have a condition, the chance that the test will come back negative.
- If a 100% specific test is positive, the patient HAS the condition.
- If a 100% specific test is negative, the patient MAY have the condition but assuming sub-par sensitivity there will be some false negatives.
(4) Absolute risk reduction.
- The reduction in the absolute risk of developing a disease over a specified time period.
- For example, if the risk of developing a disease over one year is 18% without tablet x and 12% with tablet x, the absolute risk reduction is 6%.
(5) Relative risk reduction.
- The reduction in the relative risk of developing a disease compared to a control group over a specified time period.
- Calculated as: (control event rate - experimental event rate)/control event rate.
- In the example above, the relative risk reduction for tablet x is (18-12)/18=33%.
(1) Gold standard.
- The best available diagnostic test.
(2) Sensitivity.
- If a patient has a condition, the chance that the test will come back positive.
- If a 100% sensitive test is positive, the patient MAY have the condition but assuming sub-par specificity there will be some false positives.
- If a 100% sensitive test is negative, the patient DOES NOT have the condition.
(3) Specificity.
- If a patient does not have a condition, the chance that the test will come back negative.
- If a 100% specific test is positive, the patient HAS the condition.
- If a 100% specific test is negative, the patient MAY have the condition but assuming sub-par sensitivity there will be some false negatives.
(4) Absolute risk reduction.
- The reduction in the absolute risk of developing a disease over a specified time period.
- For example, if the risk of developing a disease over one year is 18% without tablet x and 12% with tablet x, the absolute risk reduction is 6%.
(5) Relative risk reduction.
- The reduction in the relative risk of developing a disease compared to a control group over a specified time period.
- Calculated as: (control event rate - experimental event rate)/control event rate.
- In the example above, the relative risk reduction for tablet x is (18-12)/18=33%.
Conclusion
A proper history, examination, and understanding the relative impacts of tests and treatments are a good start. However, the comprehensive neurologist goes further by conducting and interpreting his or her own tests on nerves and muscles.