Introduction of neurology

Introduction to Neurology

Prof Akram Al-Mahdawi CABM,DM,MRCP,FRCP,FACP,FAAN


Meridians of Longitude= motor pathway, sensory pathways (Vibration &proprioception, pain & temperature). Parallels of Latitude( Cortex---muscle)

Nine Syndrome Patterns

Muscle Neuromuscular junction Peripheral nerve Nerve root Spinal cord Cerebellum Brainstem Sub-Cortical Cortical


1. Muscle – Proximal symmetric weakness without sensory loss HistoryLower Ext – difficulty rising from sitting positionUpper Ext – difficulty lifting grocery bags, small children etc.,Normal sensation – may have myalgia or cramps

1. Muscle (con’t.) ExamProximal symmetric weakness without sensory lossMuscles – normal size, no atrophy or fasciculations -- Tone are normal to slightly decreased

Proximal Weakness

2. Neuromuscular Junction Resembles muscle: proximal variable weakness
History Fatigability (waxing and waning weakness) Patient fatigues with prolonged activity (myasthenia gravis) Patient strength improves with activity (myasthenia syndrome)



2. Neuromuscular Junction (con’t.) Exam – resembles muscle (proximal weakness)Fatigability of proximal muscles without sensory lossLooses strength after exercise (eg., ptosis after sustained upward gaze)Muscles normal size, no atrophy or fasciculationsNormal tone

Variable Weakness

3. Peripheral Nerve Distal Weakness
HistoryLower ext – trips, drags feet, wears out toes of shoesUpper ext – drops objects, problems with gripAsymmetric weakness – localized to involved nerve (compression syndromes)Symmetric weakness – secondary to metabolic changes (eg., diabetes, renal etc)Muscle atrophySensory changes - paresthesias

3. Peripheral Nerve (con’t.) ExamDistal weakness Atrophy Sensory lossMuscle tone normal or slightly decreasedReflexes decreasedAutonomic changesTrophic changes – smooth shinny skinVasomotor changes – swelling or temperature dysregulation, loss of hair or nails

4. Nerve Root *Pain is the hallmark

History – sharp, stabbing, hot, electric, shooting or radiating painResembles peripheral nerve but weakness may be proximal or distal depending on the involved nerve rootLower ext L5 – S1 is most common; distalUpper ext C5-C6 is most common: proximal

4. Nerve Root (con’t.) Exam Distal often asymmetric weakness Atrophy and fasciculations Tone normal or decreased reflexes decreased or absent in involved muscles Sensory loss (dermatomal) Maneuvers that stretch the nerve root increase pain ( eg., valsalva, )

Clinical Findings in Upper and Lower Motor Neuron Defects

Upper motor neuron defectSpastic weaknessNo significant muscle atrophyNo fasciculations and fibrillationsHyperreflexiaExtensor planter (Babinski’s reflex)Lower motor neuron defectFlaccid weaknessSignificant atrophyFasciculations and fibrillationsHyporeflexiaFlexor planter respon


5. Spinal Cord - Triad of Symptoms
1. Sensory level - Pathognomonic 2. Distal symmetric-weakness 3. spastic weakness (UMN) 4. Bladder and bowel dysfunction due to autonomic fibers in spinal cord


5. Spinal Cord (con’t.) History Lower ext. weakness – drags toes or tripsUpper ext. weakness – drops objects or problem with gripSymmetric – both legs or both arms and legs equallySensory complaint – belt, band, girdle or tightness around trunk or abdomenSphincter dysfunction – retention or incontinence of bladder more common than bowel

5. Spinal Cord (con’t.) Exam Sensory level (tested with pinprick) Weakness more common in legs than arms Urinary retention or incontinence Superficial reflexes decreased (anal wink, bulbocavernosus and cremasteric) UMN damage - distal > proximal weakness (weakness of extensor and (anti-gravity muscles greater than flexors)


6. Brainstem – Ipsilateral cranial nerve and contralateral long tract signs History Long tracts (hemiparesis or hemisensory loss) Cranial nerves (the 6 Ds) Diplopia Dysarthria Dysphagia Dizziness Deafness Decreases strength or sensation over the face (crossed signs may be bilateral)


6. Brainstem (con’t.) ExamCranial nerves Ipsilateral -ptosis, pupillary abnormality, extraocular paralysis, diplopia, nystagmus, decreased corneal and blink reflexes, facial weakness or numbness, deafness, vertigo, dysarthria, dysphagia, weakness or deviation of the palate, decreased gag reflex, weakness of neck, shoulders or tongueLong tracts – Contralateral distal extensor (UMN) hemiparesis, increased reflexes, spasticity, Babinski, loss of some and possibly all modalities

Neurologic Examination when Brainstem is Lesioned

Higher Cortical Function: normalCranial Nerves:III, IV, VI: diplopiaV: decreased facial sensationVII: droopingVIII: deaf and dizzyIX, X, XII: dysarthria and dysphagiaXI: decreased strength in neck and shouldersCerebellar Function: normalMotor: hemi-paresis, UMNSensory: hemi-dysesthesiasDeep Tendon Reflexes: hemi-hyper-reflexiaPathologic Reflexes: Babinski’s reflex

7. Cerebellum - In-coordination, clumsiness, intention tremor *(smooths and refines voluntary movements)
HistoryClumsiness in lower ext. –staggers, drunken walkClumsiness in upper ext. – difficulty with targeting movements (such as lighting cigarettes, keys in car ignition) and intention tremorBrainstem symptoms are common with cerebellar disease and vice versa

7. Cerebellum (con’t.) ExamLower Ext. - Gait (staggering, wide based, ataxic, difficulty with tandem walking, Heel-shin, or tracing patterns on floor with toeUpper ext. – Intention tremor, difficulty targeting movements (such as finger-nose, heel shin) difficulty with rapid alternating movements (dysdiadochokinesis)


Sub-cortical v Cortical (con’t.) 1.Specific Cortical DefectsLanguage (dominant hemisphere)Speech – aphasiaWriting – agraphiaReading – alexiaComprehension (eg., apraxia)Visual-spatial (Non-dominant hemisphere)Denial or neglect of physical signs and symptoms (agnosia)


Sub-cortical v Cortical (con’t.) 2. Patterns of motor & sensory defects Cortical lesions - complete paralysis or sensory loss of face and arm (spares legs)Subcortical lesions – complete paralysis or sensory loss of face, arm, trunk and legs

Sub-cortical v Cortical (con’t.) 3. Type of sensory defect *(most primary sensory modalities reach consciousness in the thalamus and do not require the cortex for their perception)Cortical lesions – patients can still feel pain, touch, vibration and position but have impaired higher sensory processing, ie., graphesthesia or astereognosis)Subcortical defect – patient complains of significant numbness

Sub-cortical v Cortical (con’t.) Exam 1.Cortical – aphasia, visual-spatial dysfunction or seizures2.Motor – UMN weaknessCortical - Face and arm Sub-cortical - Face, arm, trunk and leg

Cortical Brain

Depends upon hemispheric dominance Non-neurologists generalize: right: visual/spatial, perception and memory left: language and language dependent memory Look for aphasias, apraxias, and agnosias


Sub-cortical v Cortical (con’t.) Exam 3. SensoryCortical – impaired higher sensory processing, (eg.,graphesthesia or astereognosis) with relatively normal sensationSub-cortical – decrease primary sensory modalities, (eg., pinprick and touch etc.,)4.VisualCortical – no defect unless occipital lobeSub-cortical – visual field defects