Functional Distinctions

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Charles Carpenter
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1 Functional Distinctions FUNCTION COMPONENT DEFICITS Start Basal Ganglia Spontaneous Movements Move UMN/LMN Cerebral Cortex Brainstem, Spinal cord Roots/peripheral nerves Plan Cerebellum Ataxia Adjust Cerebellum Ataxia Weak/Paralyzed Balance/EyeMove Cerebellum Loss of balance Nystagmus

2 Can you recognize symptoms Can you identify the motor component involved Can you localize to the site of injury

3 UMN/LMN

4 Origin of Corticospinal Tracts

5 UMNs for body Corticospinal Tract Cortico-Bulbo-Spinal Tracts UMNs involve 2 components: 1. CST - responsible for limb movements 2. CBST - influences stretch reflex and posture

6 Corticospinal Tract Post limb of internal capsule Crus cerebri of midbrain Basilar pons Pyramids of medulla Lateral corticospinal tract

7 LMNs for Body Muscle tone and DTR amplitude are clinical indicators of entire motor system. lateral motor column motor column

8 Symptoms of Lesions LMN Lesions 1.Weakness/paralysis 2. Decreased tendon reflexes 3.Decreased muscle tone- Flaccid 4. Severe muscle atrophy 5. Fasciculations UMN Lesions 1. Weakness/paralysis 2. Increased muscle tone- Spasticity 3. Increased tendon reflexes 4. Babinski sign

9 Brainstem LMNs midbrain Cranial Nerve Motoneurons: CN III, IV extrinsic eye muscles pons medulla CN V jaw muscles CN VI CN VII facial muscles CN IX, X = Nucleus Ambiguus for larynx, pharynx CN XII tongue midbrain pons medulla spinal cord CN XI trapezius, sternocleidomastoid

10 Motor Cranial Nerve Lesions Cranial Nerve Lesions ipsilateral weakness CN III, IV, VI CN V CN VII Nuc Ambiguus CN XII weakness of extrinsic eye muscles jaw deviates to weak side weakness of facial muscles loss of gag reflex/swallowing, hoarseness, uvula deviates to strong side; palate droop tongue deviates to weak side CN XI weakness in shoulder shrug, weakness turning head to opposite side Midline structures often deviate to one side when muscles are weak/paralyzed on one side.

11 Corticobulbar Fibers UMN CST CN III, IV, VI gaze centers Bilateral CN V CN VII motoneurons of upper face Contralateral CN VII to motoneurons of lower face CN XII V VII XII Nuc ambiguus travel together

12 Corticobulbar/Corticospinal Lesions For UMN Lesion on RT Side opposite lesion: drooping mouth decreased nasolabial fold tongue deviates But with normal forehead muscles eye blink drooping of mouth tongue deviates to weak side??

13 Brainstem lesions that involve both the corticospinal tract and a cranial nerve nucleus or its fibers produce a classic symptom known as alternating hemiplegia Paralysis of the body on the side opposite the lesion + cranial nerve deficit on the same side as the lesion. This is a localizing symptom indicating 1. lesion is in brainstem 2. lesion is at level of CN involved midbrain pons medulla

14 Basal Ganglia

15 Components 1. Caudate 2. Putamen }Striatum 3. Globus Pallidus 4. Substantia Nigra 5. Subthalamic Nucleus

16 Circuit Summary CST CBT SNc VL accelerator brake STN SN cdopamine The thought to move initiates a small amount of activity in cortical motor areas. Axons from cortex excite putamen neurons. Simultaneously, SN releases dopamine into putamen, which increases the effect of the accelerator and removes the brake. VL activity increases and its axons further excite cortical motor areas where CST/CBT neurons now have enough activity to cause movement.

17 Symptoms of BG Diseases Dyskinesias movement disorders hemiballismus chorea dystonia/athetosis resting tremor Hypokinesia / Bradykinesia Rigidity lead pipe with cogwheeling Changes in posture

18 Basal Ganglia Diseases Disease Lesion Site Symptoms Hemiballismus Subthalamic N Wild,flailing movements Parkinson s Huntington s Tardive dyskinesia Sub Nigra c Depletes dopamine release into putamen Caudate/Putamen Degeneration of putamen neurons with D2 recep indirect circuit Blockade of D2 receptors by drugs resting tremor, bradykinesia, rigidity, altered gait/posture Chorea, dementia Facial chorea/athetosis Tourettes s unknown Motor and verbal tics Wilson s Disease, CO poisoning

19 Cerebellum

20 Functional Units Vestibulocerebellum nodulus and flocculus Spinocerebellum Vermis / Hemisphere Cerebrocerebellum Hemisphere

21 Symptoms of Cerebellar Lesions Flocculus/Nodulus Vermis Cerebellar Hemisphere Vestibular Signs Ataxia - Truncal Ataxia - upper/lower limb falling ataxic gait nystagmus nausea, vertigo ataxic gait intention tremor, dysmetria, dysdiadochokinesia, dysarthria, etc 4th ventricle tumors Alcohol, MS, tumor Tumor, infarct, MS

22 In a nutshell Cerebellar symptoms include: vestibular signs and ataxia Flocculus/nodulus lesions cause vestibular symptoms Vermis lesions cause truncal ataxia Hemisphere lesions cause limb ataxia Cerebellar damage causes ipsilateral motor deficits. Cerebellar symptoms are caused by damage to the cerebellum, its peduncles, any of its pathways. WHAT TO KNOW?

23 Pathways Communicating with Cerebellum dorsal spinocerebellar tract ventral spinocerebellar t

24 OY - So Many Pathways

CN V! touch! pain! Touch! P/T!

CN V! touch! pain! Touch! P/T! Visual Pathways! L! R! B! A! C! D! LT! E! F! RT! G! hypothalamospinal! and! ALS! Vestibular Pathways! 1. Posture/Balance!!falling! 2. Head Position! 3. Eye-Head Movements