Lecture 7: Cerebellar and Balance Disorders PDF

Lecture 7: Cerebellar and Balance Disorders Overview: ● Develops from the alar plates (rhombic lips) of the metencephalon ● Located infratentorially within posterior fossa & lies between the temporal, occipital lobes & BS ● 3 primary functions: ○ Maintenance of posture ○ Maintenance of muscle tone ○...

Lecture 7: Cerebellar and Balance Disorders Overview: ● Develops from the alar plates (rhombic lips) of the metencephalon ● Located infratentorially within posterior fossa & lies between the temporal, occipital lobes & BS ● 3 primary functions: ○ Maintenance of posture ○ Maintenance of muscle tone ○ Coordination of voluntary motor activity Anatomical subdivisions: ● Cerebellum surface has numerous parallel folds (folia), oriented in the transverse plane ● Folia sharing a common stem of white matter form a lobule ● Ten lobules form the cerebellar cortex ● In the sagittal plane the cerebellum consists: ○ Vermis → median part ○ Lateral hemispheres ○ Each hemisphere divided: ■ Paravermal or intermediate ■ Lateral parts ■ The lateral hemisphere is largest in the posterior lobe ● Covered by a 3 layered cortex → contains folia & fissures ● Contains central medullary core, a white matter that contains: ○ Myelinated axons ○ Cerebellar nuclei (dentate, emboliform, globose & fastigial nuclei) ■ Emboliform & globose nuclei = interposed nucleus Functional areas of the cerebellar cortex: Fastigial nuclei (vermis) & Vestibular nuclei (flocculonodular lobe) ● Control of proximal trunk muscles & vestibule-ocular control (balance) ● Lesion at the vermis: loss/weakness of control of proximal & trunk muscles ● ● ● ● Interposed nuclei (emboliform & globose) in intermediate zone ● Control distal muscle in arm & legs ● Injury → ataxia ● Lateral corticospinal tract ● Rubrospinal tract Dentate nuclei (lateral hemisphere) ● Planning the motor program for extremities ● Lateral corticospinal tract Anterior corticospinal tract Reticulospinal tract Vestibulospinal tract Tectospinal tract 3 LOBES: Anterior (spinocerebellum): ● Lies anterior to the primary fissure ● Receives input from stretch receptors (muscle spindles) & GTO via spinocerebellar tracts ● Role: regulation of muscle tone Posterior (neo/pontocerebellum): ● Lies between primary fissure & posterolateral fissure ● Receives input from neocortex via the corticopontocerebellar fibers ● Role: coordination of voluntary motor activity Flocculonodular (vestibulocerebellum): ● Consists of nodulus (of the vermis) & flocculus ● Receives input from the vestibular system ● Role: maintenance of posture & balance Manifestations of cerebellar diseases: Characterized by hypotonia, disequilibrium & dyssynergia ● Hypotonia: ○ Loss of resistance normally offered by muscles to palpation or to passive manipulation ○ Results from loss of cerebellar facilitation of the motor cortex via tonic firing of cerebellar nuclei ○ Results in a floppy, loose-jointed, rag-doll appearance with pendular reflexes ○ Pt appears inebriated ● Disequilibrium → loss of balance, characterized by gait & trunk ataxia ● Dyssynergia: loss of coordinated muscle activity, includes the following: ○ Dysarthria → Slurred or scanning speech ○ Ataxia → lack of coordination in execution of voluntary movement (ex: gait, trunk, leg & arm) ■ Nystagmus → form of ataxia consisting of to & fro eye movements (ocular dysmetria) ○ Dysmetria → inability to arrest muscular movement at the desired point (past-pointing) (overshoots or undershoots when attempting to touch an object. ■ Intention tremor → type of dysmetria that occurs during a voluntary movement ● Dysdiadochokinesia → inability to perform rapid alternating movements (ex: rapid supination & pronation of hands) ● Decomposition of movement: ○ Consists of breaking down a smooth muscle act into a number of jerky awkward component parts ○ Rebound or lack of check ■ Results from the inability to adjust to changes in muscle tension ■ Caused by loss of the cerebellar component of the stretch reflex ■ Test: have the pt flex forearm at elbow against resistance → sudden release results in forearm striking patient’s chest Anterior lobe syndrome ● LL are affected the most ● Cause: Chronic alcoholism → damage to purkinje ● Results: gait, trunk & leg ataxia ● Heel-shin test: extremely difficult for pt to do ● If degeneration progresses posteriorly UL & speech may also be affected → dysarthria Posterior vermis syndrome & Folliculonodular lobe syndrome ● Involves flocculonodular lobe ● Cause: brain tumors in children ● Mcc by medulloblastomas arising in 4th ventricle or ependymomas ● Results: truncal ataxia walk on wide base Cerebellar hemispheric syndrome ● Usually involves one hemisphere ● Cause: brain tumor or abscess ● Results: arm, leg, trunk & gait ataxia ipsilateral to the lesion Posterior lobe syndrome (neocerebellar) ● Cause: strokes, tumors, trauma, degenerative disease (ex: Fredrick’s ataxia → these pts have cardiomyopathy & DM) ● Manifested by: ○ Ataxia & ↓ muscle tone ○ Intention tremor: ■ Only when voluntary movement not at rest ■ Most severe → damage to dentatothalamic tract ■ In multiple sclerosis ■ Midbrain infarctions ○ Dysmetria & Dysdiadochokinesia ○ Dysarthria → pt attempt to compensate by breaking words into syllables & uttering them with great force (explosive speech) Symptoms of cerebellar disease: VANISHD Vertigo, Ataxia, Nystagmus, Intention tremor, Slurred speech, Hypotonia, Dysdiodochokinesia ● Vertigo (spinning sensation) ● Nausea & vomiting ● Dysarthria (slurred speech) ● Headache (occipital, frontal or upper cervical ipsilateral to the lesion) ○ Hydrocephalus can lead to headache ● Ataxia ○ Disordered contractions of agonist & antagonists' muscles & lack of normal coordination between movements at different joints ○ Movements have an irregular, wavering course that seems to consist of continuous overshooting, overcorrecting & then overshooting again around the intended trajectory ○ Ataxic movements have abnormal timing (dysrhythmia) & abnormal trajectories through space (dysmetria) ○ Truncal ataxia: ■ Lesions → cerebellar vermis affect primarily the medial motor systems ■ Bilateral disorder ■ Wide-based, unsteady, “drunk-like” gait with no other significant abnormalities on exam ■ Tend to fall or sway toward the side of the lesion ■ Severe → may have difficulty sitting up without support ○ Appendicular ataxia: ■ Lesions → intermediate & lateral portions of cerebellar hemisphere affect lateral motor systems ■ Ataxia on movement of the extremities ○ Ipsilateral localization of ataxia: ■ Afferent & efferent cerebellar connections involved in the lateral motor systems either are ipsilateral or cross twice between the cerebellum & sc ○ False localization ataxia mimickers: ■ Ataxia is often caused by lesions outside the cerebellum that involve the cerebellar input or output pathways ■ Lesions of cerebellar peduncles or pons can produce severe ataxia, even without involvement of cerebellar hemispheres ■ Hydrocephalus → damage to frontopontine pathways & lesions of prefrontal cortex can both result in gait abnormalities that resemble cerebellar truncal ataxia, as can disorders of the sc ○ Often lesions extend to involve both vermis & hemispheres → truncal & appendicular ataxia coexist ○ A unilateral lesion in the lateral portion of the hemisphere may produce no appreciable deficit ○ More severe & lasting deficits are seen with lesions of intermediate hemisphere, vermis, deep nuclei, or cerebellar peduncles If we see these symptoms we suspect cerebellar disease, either acute, insidious, or chronic If acute → may suggest vascular insult (ex. Infarction) have to be dealt with immediately Titubation: paraneoplastic syndrome → nodding movement of the head or body, especially as caused by a nervous disorder. Scanning speech: post-hypoxia Truncal tremor: spinocerebellar ataxia (SCA2) Examination check slide pics <3 Kumar & clarke: Cerebellar lesions in lateral hemispheres: ● Nystagmus: coarse horizontal nystagmus develops with a lateral cerebellar lobe lesion. ○ The fast component is always towards the side of the lesion. ● Dysarthria: Halting, jerking speech (scanning speech) develops ● Titubation: rhythmic head tremor as either forward & back (yes–yes) movements or rotary (no–no) movements can occur, mainly when cerebellar connections are involved (eg. in essential tremor & MS) Cerebellar lesions in flocculonodular lobe: ● cause vertigo & vomiting with gait ataxia if they extend to the roof of the IVth ventricle