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Localization in Neurologic Diagnosis Part 1 D. Joanne Lynn, MD Associate Professor of Neurology Associate Dean of Student Life

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Presentation on theme: "Localization in Neurologic Diagnosis Part 1 D. Joanne Lynn, MD Associate Professor of Neurology Associate Dean of Student Life"— Presentation transcript:

1 Localization in Neurologic Diagnosis Part 1 D. Joanne Lynn, MD Associate Professor of Neurology Associate Dean of Student Life

2 Objectives  Be able to accurately differentiate between examination findings suggesting upper vs. lower motor neuron pathology  Correlate neurologic signs and clinical features to the appropriate level of the neuroaxis for the following neurologic localizations:  Focal cortical disease, including a gross classification of aphasias;  Cerebellar disease;  Brainstem lesions;  Spinal cord disease;  Root and peripheral nerve disease;  Neuromuscular junction dysfunction;  Myopathy

3 Objectives – continued…  Define dysarthria, dysphagia, aphasia, aphonia. Compare and contrast Broca’s, Wernicke’s, conduction and global aphasia.  List the primary functions of the frontal, parietal, temporal, and occipital lobes.  Correlate visual field deficits with lesions along the visual pathways.  Describe abnormalities of clinical eye movements that will be caused by lesions in cerebral and brainstem pathways that control eye movements.  Recognize clinical presentations that suggest brainstem pathology: grouped cranial nerve palsies, crossed motor and sensory findings.  Recognize clinical syndromes related to spinal cord pathology based on examination findings of motor and sensorydeficits.  Identify motor, sensory and reflex abnormalities that occur in C6, C7, C8, L5 and S1 radiculopathies.

4 Holism vs. Cortical localization Holism – all parts of the brain are similar in function, undifferentiated and work together as an aggregate field Localism – the concept that specific neurons and areas of the brain have specific functions Connectionism – a view that mental or behavioral phenomena are the product of interconnected networks of simple units.

5 Cortical Localization vs. Holism  Phineas Gage – 1848  Broca and M. Leborgne – 1861  Wilder Penfield – electrical stimulation results  Animal ablation studies  Functional studies by PET – 1990s

6 Phineas Gage and the frontal lobe

7 Paul Broca and M. Leborgne’s brain

8 Learning localization via pathological observations

9 Wilder Penfield and Cortical Mapping

10 Penfield and cortical mapping

11 PET scan and mapping

12 LOCALIZATION IN NEUROLOGIC DIAGNOSIS Joanne Lynn MD

13 Levels of the nervous system Central Nervous System Cerebrum / cortex Basal ganglia Cerebellum Brainstem Spinal Cord Peripheral Nervous System Roots Plexus Peripheral nerves Neuromuscular junction Muscle

14 Anatomical Localization  History and physical examination  Can the findings be explained by:  One lesion?  Multiple discrete lesions?  A diffuse process?  What level / levels of nervous system are affected?  Beware false localizing signs, non-physiologic (functional) disease

15 Levels of the nervous system

16 Let’s start at the top with the cerebral cortex

17 Important cortical areas for clinical diagnosis

18 Cortical Functions - Language  Aphasia/dysphasia – true language disturbance with errors of grammar, word production and / or comprehension This should be differentiated from disorders of speech production:  Dysarthria – disorder of articulation due to the motor function underlying speech in which language is intact  Dysphonia – impairment of the ability to produce sounds due to disorder of larynx or its innervation  Aphonia – total loss of voice often due to bilateral recurrent laryngeal nerve injury, resection of larynx, etc.

19 Cerebral Dominance / Lateralization  90% of the population is definitely right handed  99% of these are strongly left hemisphere dominant for language  The 10% who are left-handed are different:  80% have some degree of language representation in both hemispheres

20 Language testing  Handedness  Spontaneous speech: fluency, articulation, prosody, grammar, errors (paraphasias)  Comprehension: single words, yes/no questions, complex commands  Repetition  Naming  Reading/ Writing

21 Broca’s aphasia  Lesion in dominant inferior frontal gyrus  Nonfluent aphasia  Comprehension good  Associated contralateral hemiparesis if nearby motor strip is involved

22 Wernicke’s aphasia  Lesion in dominant superior temporal gyrus  Speech fluent but nonsensical  Poor auditory comprehension  Poor awareness of problem

23 Aphasia- Localization

24 Vascular supply related to aphasias

25 Frontal Lobe  Hemiparesis  Personality changes: Apathy, euphoria, jocularity, irritability, social inappropriateness  Decreased executive functions  Frontal micturation area – 2 nd frontal gyrus – may develop urinary incontinence (as in NPH)  Disorders: tumors, head trauma, hydrocephalus  Tests: alternating sequences alternating motor patterns `fist-palm-side test

26 Descending Corticospinal and Corticobulbar tracts

27 Alternating sequencing tasks – impaired in extensive frontal lobe disease

28 Frontal lobe function: alternating sequences: Fist, side, palm

29 Temporal Lobe  Bilateral lesions: profound memory loss  Dominant side: decreased verbal learning  Nondominant side: decreased visual learning  Visual field defects  Most common site of seizure focus for partial seizures

30 Temporal lobe and memory

31 Parietal Lobe  Either side: disturbance of sensation on the opposite side of the body Central sensory functions:  Decreased 2 point discrimination  Sensory inattention / extinction  Sensory agnosia:  Astereognosis  Agraphesthesia

32 Parietal Lobe Pain pathways – Spinothalamic tract to thalamus To parietal lobe

33 Parietal Lobe Vibration and proprioception input Posterior or dorsal columns To Nucleus gracilis and cuneatus To Thalamus To Parietal lobe

34 Parietal Lobe Syndromes  Dominant hemisphere:  Apraxias – inability to carry out an action in response to verbal command in the absence of problems with comprehension, impairment of motor function.  Gerstmann’s syndrome: impaired calculation, left-right confusion, finger agnosia, dysgraphia  Nondominant hemisphere:  Neglect of opposite side  Impaired constructional ability

35 Neglect – parietal lobe dysfunction

36 Occipital lobe 

37 Visual system Optic nerves, tracts, Radiations and cortex And associated visual field defects

38 Laughter is the best medicine

39 Basal ganglia  A whole set of clinical neurologic problems may be associated with lesions of the basal ganglia.  Clues to this localization include:  Some types of tremor  Rigidity  Hypokinesia or hyperkinesia  Postural disturbances  Many movement disorders caused by dysfunction in this system are not associated with dramatic abnormalities on routine imaging – so the clinician must recognize typical syndromes by clinical features on history and exam.

40 Cerebellum

41 Cerebellum – clinical signs  Incoordination  Dysdiadochokinesis  Terminal dysmetria  Intention tremor  Truncal and appendicular ataxia  Hypotonia  Rebound  Oculomotor abnormalities  Dysarthria commons.wikimedia.org

42 Ataxia  Incoordination or clumsiness of movement not caused by weakness or sensory loss – rather caused by a disordered contractions of paired agonist and antagonist muscles  The word ataxia derives from Greek words meaning ‘lack of order’  Localization:  True ataxia is Cerebellar  Sometimes people speak of Vestibular ataxia or Sensory (proprioceptive) ataxia because they are also associated with staggering gait/ loss of balance  So beware that this is a word that may mean different things to different speakers

43 Cerebellar modulation Of descending Corticospinal tract

44 Brainstem level localization

45 Brainstem – Clues to Brainstem Localization  Grouped cranial nerve findings  Brainstem site  Site within skull  Generalized disorder of nerve, NMJ  Divergent eye movements with diplopia  Vertigo  Discrepancies in lateralization of motor or sensory deficits – alternating sensory or motor findings  Look for well-defined syndromes – like brainstem strokes

46 Brainstem wiring for eye movements

47 FACIAL PALSIES – PLEASE LOCALIZE AS UPPER VS. LOWER MOTOR NEURON LESIONS Joanne Lynn MD

48 Facial palsy on the right….

49 Left facial palsy Woman with a peripheral facial palsy – note that the Left side of the forehead does not wrinkle while the right does.

50 Brainstem stroke syndromes and localization

51 Midbrain stroke syndromes

52 Laughter is the best medicine

53 Spinal Cord

54 Simplified spinal cord for clinical case analysis

55 Spinal cord syndromes  Complete transverse lesion  Hemisection (Brown- Sequard)  Posterior column loss  Anterior spinal syndrome  Central cord syndrome

56 Remember crossing of pain and temperature fibers in cord

57 UMN vs LMN signs  Upper motor neuron signs:  Increased tone spasticity  Hyperreflexia  Extensor plantar response  Lower motor neuron signs:  Decreased tone  Hyporeflexia  Flexor plantar response  Muscle atrophy, fasciculations

58 Atrophy of Interossei muscles Atrophy is more prominent with weakness of LMN etiology

59 Reflexes  Myotatic stretch reflexes  Monosynaptic reflex: stretch muscle, stimulate Ia sensory afferent, stimulate alpha motorneuron AnkleS1, S2 PatellarL3, L4 BicepsC5, C6 TricepsC7, C8

60 Reflex arc

61 Stupid Neurology cartoon

62 Come back for Part 2 – It is much shorter!

63 Thank you for completing this module Questions? Contact me at:

64 Survey We would appreciate your feedback on this module. Click on the button below to complete a brief survey. Your responses and comments will be shared with the module’s author, the LSI EdTech team, and LSI curriculum leaders. We will use your feedback to improve future versions of the module. The survey is both optional and anonymous and should take less than 5 minutes to complete. Survey


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