# Lecture 17: Neurological Examination ## Unit 2.5: Neuroscience --- ## Learning Objectives By the end of this lecture, students will be able to: 1. Describe the systematic approach to the neurological examination 2. Explain the mental status examination components 3. Describe the examination of motor and sensory systems 4. Explain reflex testing and its clinical significance 5. Describe cerebellar and gait examination 6. Apply examination findings to neurological localization --- ## Lecture Outline ### I. Overview and Systematic Approach The neurological examination is a systematic assessment of the nervous system that localizes lesions and guides diagnosis. It comprises seven main components: mental status, cranial nerves, motor system, sensory system, reflexes, coordination, and gait. Each component assesses different parts of the neuraxis, and abnormalities are interpreted in the context of neuroanatomical pathways. A complete neurological examination takes considerable time, so clinicians typically perform focused examinations based on the patient's presenting symptoms while maintaining awareness of what a complete examination would include. The fundamental principles of the neurological examination include systematically examining the same components in the same order to avoid omissions, always comparing right to left (asymmetry is often more significant than bilateral abnormality), observing the patient before formal testing (spontaneous movements, facial expression, and gait reveal much), allowing the history to guide examination focus, and documenting findings precisely for future comparison. The examination should be tailored to the clinical situation: a screening examination for patients without neurological complaints differs substantially from the detailed assessment required for suspected stroke or multiple sclerosis. A screening neurological examination can be accomplished efficiently by checking mental status during history-taking, testing key cranial nerves (visual acuity and fields, pupillary response, eye movements, facial symmetry, and tongue protrusion), assessing motor function with pronator drift and gross strength, checking light touch and vibration sense, testing reflexes at two levels, and observing coordination with finger-to-nose testing and gait. This screening takes only a few minutes but can detect most significant abnormalities. The complete neurological examination is indicated when the patient has neurological symptoms such as weakness, numbness, headache, or cognitive changes; when altered mental status is present; following head or spinal trauma; before neurosurgery; and for follow-up of known neurological conditions. The findings are interpreted through the lens of neuroanatomy to localize the lesion and guide further workup. Neurological examination overview: Panel 1 - Flowchart showing seven examination components (mental status, cranial nerves, motor, sensory, reflexes, coordination, gait) with what each assesses: cortical function, brainstem, pyramidal/extrapyramidal systems, sensory pathways, spinal segmental levels, cerebellum, and integrated function. Panel 2 - Screening examination sequence: examiner performing pupil check, pronator drift testing, reflex hammer on patellar tendon, finger-to-nose, and observing tandem gait. Panel 3 - Documentation template showing organized recording format for each examination component. Panel 4 - Decision tree for when to perform screening vs complete examination based on clinical presentation. --- ### II. Mental Status Examination The mental status examination assesses cortical and subcortical function. It begins with evaluation of level of consciousness, ranging from fully alert through lethargic (drowsy but easily arousable), obtunded (requires repeated stimulation to arouse), stupor (only vigorous stimulation produces arousal), to coma (completely unarousable). Consciousness reflects the integrity of the ascending reticular activating system in the brainstem and its projections to the cortex. Attention is the gateway to other cognitive functions and must be intact for meaningful cognitive testing. Simple attention is tested with digit span (normal is at least 5 forward), while concentration is assessed with serial 7s (subtracting 7 from 100 sequentially), spelling WORLD backward, or reciting months in reverse. Patients with poor attention will also appear to have memory and language deficits, so attention must be evaluated first. Orientation tests awareness of person (name, age, date of birth), place (hospital, city, state), time (date, day, month, year, season), and situation (why they are being evaluated). Disorientation follows a characteristic pattern, with time lost first, then place, and finally person. Memory testing includes immediate recall (repeating a word list), recent memory (delayed recall of those words after several minutes), and remote memory (biographical facts and historical events). Language evaluation encompasses fluency (quantity and ease of speech production), comprehension (following commands of increasing complexity), repetition (repeating phrases), and naming (identifying objects). Pattern analysis localizes language deficits: non-fluent speech with preserved comprehension suggests Broca's area involvement, while fluent speech with impaired comprehension suggests Wernicke's area. Standardized assessments include the Glasgow Coma Scale for acute settings, the Mini-Mental State Examination (MMSE) or Montreal Cognitive Assessment (MoCA) for cognitive screening, and the NIH Stroke Scale (NIHSS) for acute stroke evaluation. Mental status examination: Panel 1 - Consciousness levels diagram showing spectrum from alert to coma with associated arousal stimuli needed and anatomical substrate (ARAS and cortex). Panel 2 - Attention testing illustrations: examiner presenting digit span, patient performing serial 7s, showing months backward. Panel 3 - Language assessment grid showing fluency, comprehension, repetition, and naming patterns for Broca's aphasia, Wernicke's aphasia, conduction aphasia, and global aphasia with associated lesion locations. Panel 4 - Sample MoCA test form with key sections highlighted and normal vs impaired examples of clock drawing. --- ### III. Cranial Nerve Examination The cranial nerve examination tests the brainstem and specific sensory and motor pathways. A quick screening examination includes testing visual acuity with a Snellen chart or near card, visual fields by confrontation, pupillary responses to light (direct and consensual), extraocular movements in an H-pattern asking about diplopia, facial sensation with light touch in all three trigeminal divisions, facial motor function (smile, raise eyebrows, close eyes tightly), hearing with finger rub or whispered voice, palate elevation with phonation, shoulder shrug and head turning against resistance, and tongue protrusion. The detailed cranial nerve examination adds olfactory testing with non-irritating substances, fundoscopic examination of the optic disc, color vision testing, saccadic and pursuit eye movement assessment, corneal reflex, jaw clench and opening against resistance, Weber and Rinne hearing tests if abnormality is found, the gag reflex, and voice quality assessment. Findings should be recorded for each nerve tested. Key findings and their significance include: an afferent pupillary defect (RAPD), where the pupil paradoxically dilates when light swings to the affected eye, indicating optic nerve pathology; internuclear ophthalmoplegia (INO), where adduction fails during horizontal gaze with nystagmus in the abducting eye, indicating a lesion of the medial longitudinal fasciculus (commonly from multiple sclerosis or stroke); forehead-sparing facial weakness, indicating an upper motor neuron lesion (such as stroke) because the forehead receives bilateral cortical innervation; complete hemifacial weakness including the forehead, indicating a lower motor neuron lesion (such as Bell's palsy); and tongue deviation, which in LMN lesions points toward the weak side with ipsilateral atrophy and fasciculations. Cranial nerve examination: Panel 1 - Visual field testing by confrontation technique showing examiner and patient positioning, finger counting in each quadrant, and recording template. Panel 2 - Eye movement testing in H-pattern with diagram of which muscle is primarily tested in each gaze position. Panel 3 - Facial motor testing sequence: raise eyebrows (frontalis), close eyes against resistance (orbicularis oculi), puff cheeks (buccinator), smile (zygomaticus), with comparison of UMN vs LMN patterns. Panel 4 - Tongue examination showing normal midline protrusion, left LMN lesion with deviation to left and atrophy, and right UMN lesion with deviation to left initially. --- ### IV. Motor Examination The motor examination assesses the integrity of upper and lower motor neurons, neuromuscular junctions, and muscles. It comprises four components: inspection for atrophy, fasciculations, and involuntary movements; assessment of muscle tone; evaluation of muscle strength; and comparison of bulk between sides. These findings, combined with reflex testing, distinguish upper motor neuron from lower motor neuron pathology and help localize lesions along the motor pathway. Tone is assessed by passive movement of the limbs while the patient relaxes. Spasticity, characterized by velocity-dependent resistance with a catch and release (clasp-knife phenomenon), indicates upper motor neuron pathology and reflects loss of descending inhibition of the spinal stretch reflex. Rigidity is constant resistance throughout the range of motion regardless of velocity, seen in parkinsonian conditions. Cogwheel rigidity (ratchety quality) reflects superimposed tremor. Flaccidity, or decreased resistance, occurs with lower motor neuron lesions. Paratonia (gegenhalten) is variable, inconsistent resistance suggesting frontal lobe dysfunction or poor cooperation. Strength is graded using the Medical Research Council (MRC) scale: 0 indicates no contraction; 1 indicates a trace or flicker of movement; 2 indicates movement with gravity eliminated (sliding the limb across the bed); 3 indicates movement against gravity but not resistance; 4 indicates movement against resistance but reduced from normal (often subdivided into 4-, 4, and 4+); and 5 indicates normal strength. Testing should cover key muscle groups representing different myotomes: shoulder abduction (C5, deltoid), elbow flexion (C5-C6, biceps), wrist extension (C6-C7), elbow extension (C7, triceps), finger extension (C7), hand intrinsics (T1), hip flexion (L2-L3, iliopsoas), knee extension (L3-L4, quadriceps), ankle dorsiflexion (L4-L5, tibialis anterior), and ankle plantarflexion (S1, gastrocnemius). Pronator drift is a sensitive screening test for subtle upper motor neuron weakness. The patient holds both arms extended forward with palms up and eyes closed; the weak arm will pronate and drift downward. Patterns of weakness help localize: pyramidal (UMN) weakness is more pronounced in arm extensors and leg flexors; lower motor neuron weakness may follow a dermatomal or peripheral nerve distribution; and proximal weakness suggests myopathy. Motor examination: Panel 1 - Tone assessment technique showing examiner passively flexing and extending patient's relaxed arm at elbow, with graphs depicting normal, spastic (velocity-dependent with catch), and rigid (constant) resistance patterns. Panel 2 - MRC strength grading scale with illustrations: grade 0-1 (flicker), grade 2 (gravity-eliminated movement), grade 3 (against gravity), grade 4 (against resistance), grade 5 (normal). Panel 3 - Key muscle testing positions for each major myotome from C5 to S1 with examiner positioning and direction of resistance. Panel 4 - Pronator drift test showing normal position (palms up) and abnormal drift (pronation and downward drift of weak arm). --- ### V. Sensory Examination The sensory examination tests the integrity of peripheral sensory receptors, peripheral nerves, dorsal root ganglia, spinal cord pathways, brainstem, thalamus, and sensory cortex. Different sensory modalities travel by distinct pathways: light touch and proprioception travel via the dorsal columns and medial lemniscus, while pain and temperature travel via the spinothalamic tract. Dissociated sensory loss, where one modality is impaired while another is preserved, helps localize lesions to specific spinal cord regions. Testing technique is critical for reliability. Light touch is tested with cotton or a soft brush, asking the patient to say "yes" or "now" when they feel touch while their eyes are closed, comparing sides and moving proximal to distal. Pain is tested with a sterile pin or broken wooden applicator, alternating sharp and dull ends and asking the patient to distinguish between them. Temperature can be tested with a cold tuning fork. Vibration is tested with a 128 Hz tuning fork applied to bony prominences (great toe interphalangeal joint, then moving proximal if impaired), asking the patient to report when vibration stops, comparing to the examiner's own perception. Proprioception (joint position sense) is tested by holding the sides of a distal phalanx and moving it slightly up or down, asking the patient to identify the direction. Patterns of sensory loss have localizing value. A hemisensory loss affecting face, arm, and leg on one side suggests a thalamic or cortical lesion. A sensory level, below which sensation is lost, indicates spinal cord pathology at that level. Dermatomal loss in a single dermatome suggests radiculopathy. Glove-and-stocking distribution with distal loss greater than proximal in a length-dependent pattern indicates peripheral polyneuropathy. Dissociated sensory loss with impaired pain and temperature but preserved proprioception and vibration (or vice versa) indicates specific spinal cord pathology such as Brown-Séquard syndrome or syringomyelia. Cortical sensory tests require intact primary sensation. Stereognosis is tested by having the patient identify objects by touch alone (key, coin, paper clip). Graphesthesia is tested by drawing numbers on the patient's palm and having them identify the number. Two-point discrimination tests the minimum distance at which two points are perceived as separate. Extinction is tested by simultaneously touching both sides; failure to perceive the touch on one side indicates contralateral parietal lobe dysfunction. Sensory examination: Panel 1 - Sensory pathways diagram showing dorsal column-medial lemniscus (light touch, proprioception, vibration) and spinothalamic tract (pain, temperature) with labeled anatomy and testing method for each. Panel 2 - Dermatome map for upper and lower extremities with key landmarks for each level. Panel 3 - Sensory testing techniques: vibration with tuning fork on great toe, proprioception testing showing finger positions on toe sides, two-point discrimination on fingertip. Panel 4 - Sensory loss patterns: hemibody (thalamic), sensory level (spinal cord), dermatomal (radiculopathy), glove-stocking (polyneuropathy), dissociated (Brown-Séquard). --- ### VI. Reflex Examination Deep tendon reflexes (DTRs) test the integrity of the monosynaptic reflex arc and provide information about both lower motor neurons (the reflex arc itself) and upper motor neurons (which normally modulate reflex activity). The stretch reflex involves muscle spindle activation by tendon tap, afferent signal via sensory neuron to the spinal cord, synapse on the alpha motor neuron, and efferent signal causing muscle contraction. Each reflex corresponds to specific spinal cord levels. Standard DTR testing includes the biceps reflex (C5-C6) with the examiner's thumb on the biceps tendon and tapping the thumbnail, the brachioradialis reflex (C5-C6) by tapping the distal radius, the triceps reflex (C7) by tapping the triceps tendon just above the olecranon, the patellar reflex (L3-L4) by tapping the patellar tendon with the knee relaxed and flexed, and the Achilles reflex (S1) by tapping the Achilles tendon with the foot dorsiflexed. Reflexes are graded on a 0 to 4+ scale: 0 indicates absent, 1+ indicates diminished (may be normal in some individuals), 2+ indicates normal, 3+ indicates brisk (may be normal if symmetric), and 4+ indicates clonus (sustained rhythmic contractions). Asymmetry between sides is particularly significant. Absent or diminished reflexes suggest lower motor neuron pathology at the corresponding level. Hyperactive reflexes with a spread of the reflex response suggest upper motor neuron pathology above the reflex arc level. Pathological reflexes emerge when upper motor neuron influence is lost. The Babinski sign is tested by stroking the lateral sole from heel to ball, then curving medially across the metatarsal heads. A normal response is plantarflexion of the toes; an abnormal (positive) Babinski response is dorsiflexion of the great toe with fanning of the other toes, indicating upper motor neuron dysfunction. The Hoffmann sign is tested by flicking the nail of the middle finger; a positive response is flexion of the thumb and index finger, suggesting cervical cord or UMN pathology. Clonus, rhythmic involuntary contractions elicited by sudden ankle dorsiflexion, also indicates UMN pathology. Primitive reflexes (grasp, palmomental, snout, glabellar) reappear with frontal lobe pathology or diffuse cortical disease. Reflex examination: Panel 1 - Monosynaptic reflex arc diagram showing muscle spindle → sensory neuron → spinal cord synapse → alpha motor neuron → muscle contraction, with descending UMN modulation indicated. Panel 2 - Deep tendon reflex technique for each standard reflex (biceps, triceps, brachioradialis, patellar, Achilles) with examiner hand positioning and corresponding spinal level. Panel 3 - Babinski sign testing technique and comparison of normal (flexor) vs abnormal (extensor with fanning) responses. Panel 4 - Reflex grading comparison showing UMN lesion pattern (hyperreflexia, Babinski positive, clonus) vs LMN lesion pattern (hyporeflexia or areflexia, normal plantar response). --- ### VII. Coordination Examination The coordination examination primarily tests cerebellar function. The cerebellum coordinates voluntary movement, maintains balance and posture, and contributes to motor learning. Cerebellar lesions cause characteristic findings: dysmetria (inaccurate targeting), intention tremor (tremor that worsens as the limb approaches the target), dysdiadochokinesia (irregular rhythm of rapid alternating movements), and gait ataxia. The cerebellum exerts ipsilateral control, so unilateral cerebellar lesions cause ipsilateral findings. Limb coordination tests include finger-to-nose testing, where the patient alternates between touching their nose and the examiner's finger, which is moved to different positions. The examiner observes for dysmetria (overshoot or undershoot), intention tremor (oscillation increasing near the target), and past-pointing. Heel-to-shin testing assesses lower limb coordination; the patient runs the heel of one foot down the shin of the opposite leg, and the examiner looks for side-to-side oscillation (dysmetria). Rapid alternating movements are tested by having the patient rapidly pronate and supernate the hand on the thigh or rapidly tap the thumb and forefinger; irregular rhythm or amplitude (dysdiadochokinesia) suggests cerebellar dysfunction. The Romberg test assesses proprioceptive input to balance. The patient stands with feet together, first with eyes open, then with eyes closed. A positive Romberg sign is marked unsteadiness or falling only when the eyes are closed. This indicates a sensory (proprioceptive) ataxia because the patient can compensate for proprioceptive loss using vision, but cannot when vision is removed. Patients with cerebellar ataxia are unsteady with eyes both open and closed, so their unsteadiness does not significantly worsen when eyes close (negative Romberg). Localization within the cerebellum is possible because different cerebellar regions have different functions. Lesions of the cerebellar hemispheres cause ipsilateral limb ataxia (dysmetria, intention tremor). Lesions of the vermis cause truncal ataxia with wide-based gait and difficulty maintaining balance but relatively preserved limb coordination. The mnemonic "DANISH" helps remember cerebellar signs: Dysdiadochokinesia, Ataxia, Nystagmus, Intention tremor, Slurred speech (scanning dysarthria), and Hypotonia. Coordination examination: Panel 1 - Finger-to-nose test showing patient trajectory with normal smooth path vs dysmetric overshooting path with intention tremor oscillation near target. Panel 2 - Heel-to-shin test demonstrating proper technique with observation of smooth vs ataxic performance. Panel 3 - Rapid alternating movements (hand flip, finger tapping) showing regular rhythm (normal) vs irregular dysdiadochokinetic pattern. Panel 4 - Romberg test showing stable stance with eyes open, positive Romberg (falling with eyes closed indicating sensory ataxia), and cerebellar ataxia (unstable both eyes open and closed). --- ### VIII. Gait Examination Gait is the most integrative part of the neurological examination, requiring coordination of motor, sensory, cerebellar, vestibular, and basal ganglia systems. Observation should include initiation (hesitation or freezing), base (narrow versus wide), stride length and height, arm swing (presence and symmetry), posture (stooped or erect), turns (smooth versus en bloc), and overall stability. Specific gait patterns suggest particular diagnoses. A hemiplegic gait, seen after stroke, is characterized by circumduction of the stiff, extended leg (swinging it in an outward arc) because hip and knee flexion are weak. The arm on the affected side may be held in flexion. A parkinsonian gait features shuffling short steps, reduced arm swing, stooped posture, festination (acceleration), and en bloc turns. Starting hesitation and freezing (suddenly stopping, especially at doorways) may occur. A spastic (scissoring) gait from bilateral upper motor neuron lesions shows stiff legs with crossing of the knees during walking due to adductor spasticity. A steppage gait results from foot drop (weak ankle dorsiflexion) and is characterized by exaggerated hip flexion to lift the foot high enough to clear the ground. It may be caused by peroneal nerve palsy or L5 radiculopathy. A cerebellar ataxic gait is wide-based and lurching, with irregular stride length. Patients with cerebellar lesions cannot perform tandem (heel-to-toe) walking. A magnetic or apraxic gait, as seen in normal pressure hydrocephalus, appears as if the feet are stuck to the floor; the patient has difficulty initiating steps and takes short, shuffling steps with a wide base. Special gait tests add diagnostic information. Tandem walking (heel-to-toe along a line) is sensitive for balance and cerebellar dysfunction. Walking on heels tests ankle dorsiflexion (L4-L5). Walking on toes tests ankle plantarflexion (S1). Single-leg heel rises test S1 and calf strength. Rising from a squat without using hands tests proximal lower extremity strength; difficulty suggests hip flexor weakness (myopathy). The get-up-and-go test (standing from a chair, walking, turning, and sitting) provides a quick functional assessment, especially in elderly patients. Gait examination: Panel 1 - Normal gait components labeled: arm swing, stride length, heel strike, toe-off, narrow base, erect posture. Panel 2 - Pathological gait patterns illustrated: hemiplegic (circumduction, arm flexed), parkinsonian (stooped, shuffling, no arm swing), spastic (scissoring, stiff legs), steppage (high knee lift for foot drop). Panel 3 - Additional gait patterns: cerebellar ataxic (wide-based, lurching), magnetic/apraxic (feet stuck to floor). Panel 4 - Special tests: tandem walking, heel walking, toe walking, single-leg heel rise, and Trendelenburg sign for hip abductor weakness. --- ### IX. Localization and Pattern Recognition The goal of the neurological examination is localization—determining where in the nervous system the lesion is located. The key distinction is between upper motor neuron and lower motor neuron lesions, which have characteristic patterns. Upper motor neuron lesions (affecting the motor cortex, internal capsule, brainstem, or spinal cord above the level of the motor neurons) cause weakness with increased tone (spasticity), hyperactive reflexes, and pathological reflexes (positive Babinski). Lower motor neuron lesions (affecting the anterior horn cells, nerve roots, or peripheral nerves) cause weakness with decreased tone (flaccidity), diminished or absent reflexes, atrophy, and often fasciculations. Pattern recognition helps localize further. Hemiparesis with aphasia suggests a left cortical lesion (MCA territory). Crossed findings with ipsilateral cranial nerve deficit and contralateral body weakness indicate a brainstem lesion. Bilateral leg weakness with a sensory level and bowel or bladder dysfunction points to spinal cord pathology. Weakness in a single limb with dermatomal sensory loss suggests radiculopathy. Distal symmetric sensory loss and weakness in a stocking-glove distribution indicates polyneuropathy. Proximal weakness greater than distal with preserved sensation and reflexes suggests myopathy. Red flags requiring urgent evaluation include rapidly progressive weakness (suggesting Guillain-Barré syndrome or myasthenic crisis), ascending sensory level (suggesting cord compression), saddle anesthesia with bladder dysfunction (cauda equina syndrome), acute focal deficits (stroke), and new focal findings with fever (CNS infection). These patterns require immediate imaging and intervention. Documentation should be thorough and organized, recording findings systematically. For mental status: GCS or detailed cognitive description. For cranial nerves: individual nerve findings. For motor: MRC grades for each muscle group tested. For sensory: modalities tested and pattern of any abnormality. For reflexes: grades at each level tested and symmetry. For coordination: specific tests performed and findings. For gait: detailed description of pattern. Localization patterns: Panel 1 - UMN vs LMN lesion comparison table showing weakness (both), tone (increased vs decreased), reflexes (hyperactive vs hypoactive), atrophy (minimal vs marked), fasciculations (no vs yes), Babinski (positive vs negative). Panel 2 - Anatomical localization diagram: cortex (hemiparesis + aphasia/neglect), brainstem (crossed findings), spinal cord (bilateral with sensory level), root (dermatomal), peripheral nerve (specific distribution), NMJ (fatigable weakness), muscle (proximal). Panel 3 - Emergency patterns: cauda equina syndrome (saddle anesthesia, bilateral leg weakness, urinary retention), cord compression (sensory level, bilateral weakness), acute stroke (sudden focal deficit). Panel 4 - Documentation template showing organized recording format for complete neurological examination. --- ### X. Special Populations and Functional Assessment Examination of comatose patients requires modification because the patient cannot cooperate with testing. Assessment focuses on level of consciousness using the Glasgow Coma Scale (eye opening, verbal response, motor response), brainstem reflexes (pupillary, corneal, oculocephalic, caloric, gag), motor responses to painful stimuli (purposeful movement, withdrawal, posturing), and respiratory pattern. The oculocephalic (doll's eyes) reflex tests the vestibulo-ocular reflex; in an intact brainstem, the eyes move opposite to head rotation. Caloric testing with cold water in the ear normally produces nystagmus; in coma, the fast phase is lost and eyes deviate toward the cold ear if the brainstem is intact. Pediatric neurological examination must be adapted to developmental stage. In neonates, primitive reflexes (Moro, grasp, rooting) are normally present and their absence is abnormal. In infants, developmental milestones serve as benchmarks for neurological function. In young children, observation of play and creative testing strategies are needed to assess strength and coordination. Elderly patients may have normal age-related findings that should not be interpreted as pathological. Mild reduction in vibration sense at the ankles is common with aging due to large-fiber sensory neuron loss. Absent ankle reflexes may be normal. Slightly stooped posture and mildly slowed gait can occur with normal aging but should be distinguished from parkinsonian features. The examination for functional (psychogenic) neurological symptoms requires specific techniques. The Hoover sign tests for functional leg weakness: when asked to lift the weak leg, the strong leg normally presses down involuntarily (hip extension synergy). If this is absent when the weak leg is lifted but present when the strong leg is lifted, the weakness is likely functional. Give-way weakness shows sudden complete release during strength testing rather than gradual giving way. Distraction testing involves assessing function while the patient is focused elsewhere; inconsistency between examined and observed function suggests functional etiology. Special populations: Panel 1 - Coma examination protocol: GCS scoring table, brainstem reflex testing (pupillary, corneal, oculocephalic, caloric) with diagrams, motor responses (purposeful, withdrawal, decorticate, decerebrate posturing). Panel 2 - Pediatric developmental milestones with expected neurological findings at each age (newborn, 3 months, 6 months, 1 year). Panel 3 - Normal aging changes: mildly decreased distal vibration sense, absent ankle jerks, slight gait slowing, distinguishing features from pathology. Panel 4 - Functional examination techniques: Hoover sign showing hip extension synergy testing, give-way weakness pattern, and distraction testing example. --- ## Summary - The neurological examination comprises mental status, cranial nerves, motor, sensory, reflexes, coordination, and gait, performed systematically and comparing sides - Mental status evaluation includes consciousness level, attention, orientation, memory, and language; standardized tools include GCS, MMSE, MoCA, and NIHSS - Motor examination assesses tone (spasticity indicates UMN, flaccidity indicates LMN), strength (MRC scale 0-5), and bulk; pronator drift detects subtle weakness - Sensory examination tests dorsal column modalities (vibration, proprioception) and spinothalamic modalities (pain, temperature); patterns of loss localize lesions - Deep tendon reflexes are graded 0-4+; hyperreflexia with Babinski indicates UMN lesion; hyporeflexia indicates LMN lesion - Coordination testing (finger-nose, heel-shin, rapid alternating) assesses cerebellar function; Romberg tests proprioceptive versus cerebellar ataxia - Gait patterns are diagnostic: hemiplegic (circumduction), parkinsonian (shuffling), steppage (foot drop), ataxic (wide-based) - UMN lesions cause weakness with spasticity, hyperreflexia, and Babinski; LMN lesions cause weakness with atrophy, flaccidity, and hyporeflexia --- ## Key Terms | Term | Definition | |------|------------| | Spasticity | Velocity-dependent increased muscle tone from upper motor neuron lesion | | Rigidity | Constant resistance to passive movement throughout range (parkinsonian) | | Babinski sign | Dorsiflexion of great toe with plantar stimulation indicating UMN lesion | | Romberg test | Balance test; positive (falling with eyes closed) indicates sensory ataxia | | Dysmetria | Inaccurate targeting of movement due to cerebellar dysfunction | | Dysdiadochokinesia | Impaired rapid alternating movements from cerebellar lesion | | Pronator drift | Pronation and downward drift of outstretched arm indicating subtle weakness | | Clonus | Rhythmic involuntary contractions from hyperactive stretch reflex in UMN lesion | --- *This content is subject to the [MIT License](https://opensource.org/licenses/MIT). © 2024–2026 Hibbert School of Medicine.*