Test 7 Flashcards
Cerebellar hemispheres
Lateral hemispheres
Intermediate hemispheres
Superior cerebellar peduncle
- connects to rostral pons
- contains mostly efferent fibers
Middle cerebellar peduncle
- connects to pons
- contains mostly afferent fibers from cerebral cortex
Inferior cerebellar peduncles
- connects to cuadal pons/rostral medulla
- contains mostly afferent fibers from BS and SC
- contains efferent to vestibular nuclei and RF in brainstem
Cerebellum
- detects movement that deviates from the intended cortical command.
- smoothly coordinates ongoing movements
- contributes to motor planning
- receives massive amounts of sensory input about actual movement from the spinal cord cerebellar tracts
- integrates this sensory information and adjusts movement as necessary
Three major functions of the cerebellum:
- Synergy of movement: groups movements for the performance of selective responses
- Maintenance of Upright Posture: Body position in space
- Maintenance of Tone: maintaining tone during muscle contraction
Also participates in speech articulation, respiratory movements, motor learning and possibly higher-order cognitive processes
Three functional regions of the cerebellum
Lateral hemispheres
Intermediate hemispheres
Vermis and flocculonodular lobe
Lateral hemisphere of cerebellum function
- motor planning for extremities
- lateral corticospinal tract
Intermediate hemisphere of the cerebellum function
- Function: distal limb coordination
- lateral corticospinal tract, rubrospinal tracts
Vermis and flocculonodular lobe of teh cerebellum function
- proximal limb and trunk coordination : anterior corticospinal tract, reticulospinal tract, vestibulospinal
- balance and vestibuloocular reflexes: medial longitudinal fasciculus
Input to cerebellar cortex:
- mossy fibers (excitatory)
- climbing fibers (excitatory)
—both synapse directly or indirectly on Purkinje cells. Inputs to ther cerebllar cortex also have collateral fibers that synapse on deep cerebellar nuclei
Output from cerebellar cortex:
Purkinje fibers (inhibitory)
-project to the deep cerebellar nuclei and/ or vestibular nuclei (excitatory)
Deep cerebellar nuclei serve as…
Serve as an on/off center for cerebellar output
What are the Deep cerebellar nuclei?
-Lateral to medial “Don’t Eat Greasy Foodds”
- Dentate: input from lateral hemisphere
- Emboliform: input from intermediate hemisphere
- Globase: input from intermediate hemisphere
- Fastigial: input from vermis
Vestibular nuclei
- Function in some ways like deep cerebellar nuclei
- input from inferior vermis and flocculonodular lobe
Main cerebellar output pathways
Lateral hemispheres- Dentate
Intermediate hemispheres- interposed
Vermis- fastigial
Inferior vermis and flocculonodular lobe - vestibular
Why do cerebellar lesions cause ipsilaterall deficits in coordination?
- Pathways from the cerebellum that influence the lateral motor systems and periphery are double crossed
- lesions of the vermis don’t cause unilateral deficits because medial moor systems influence bilateral proximal trunk musculature
Who sends input to the cerebellum?
- input to the cerebellum id from virtually all areas of the cerebral cortex, many sensory modalities, brainstem nuclei, and the SC
- corticopontine fibers
- input also from vestibular nuclei, RF nuclei, and inferior olivary nuclei
Corticopontine fibers
- fibers traveling from the cerebral cortex to the cerebellum
- synapse in pons, and then are called pontocerebellar fibers
Spinocerebellar pathways
- unconscious proprioception of limb movements : dorsal spinocerebellar tract (LE), cuneocerebellar tract (UE)
- unconscious information regarding activity of spinal interneurons, as well as spinal reflex circuits: ventral spinocerebellar tract (LE), rostral spinocerebellar (UE)
- each cerebellar hemisphere receives information from the ipsi limbs. Inputs either dont cross or are double crossed
Ataxia side of lesion
- ipsi to the side of the lesion
- b/c of reciprocal connection between cerebellum, brainstem, an other regions, ataxia may be seen with lesions in these other location as well
- uncoordinated movement. Disordered contractions of agonist and antagonist muscles and lack or normal coordination b/w movements at different joints. Movements have irregular, wavering course that consists of continuous overshooting and over correcting
Midline lesions of the cerebellum
-unsteady gait and eye movement abnormalities
Lesions lateral to the vermis of cerebellum
-limb ataxia
-
Three classic signs of cerebellar damage
“ANT”
Ataxia, nystagmus, and (intention) tremor (with movement)
Also could have: dysrhythmia, dysdiadochokinesia, dysmetria
- Vertigo, N/V, unsteadiness, slurred speech, HA
Dysrhythmia
abnormal timing
Dysdiasochokinesia
Abnormal rapid alternating movements
Dysmetria
Abnormal distance trajectory
UMN or LMN lesions interfering with cerebellum exam
- UMN: can cause slow, clumsy movements of extremities
- LMN: can cause weakness, tests requiring little strength can be helpful (precision finger tap)
Basal ganglia lesion affect with a cerebellar exam
-can cause slow, clumsy movements, and/or gait unsteadiness
Sensory ataxia affecting cerebellar exam
-severe loss of position sens
—sensory ataxia should improve with visual feedback
Truncal ataxia
- lesions of the vermis
- wide -based, unsteady “drunk-like” gait
-in severe cases, the patient may also have problems sitting w/o support
Appendicular ataxia
- lesions of the intermediate or lateral cerebellum
- uncoordinated movement of the extremities
Lesions can involve vermis and both hemispheres
-intention tremor, patient attempts to move limb toward a target, produces irregular, oscillating movements in multiple planes through the trajectory
Ipsilateral localization of ataxia
-lesions of the cerebellar hemispheres cause ipsilateral ataxia of the extremities
-truncal ataxia is a bilateral disorder
—
False localization of Ataxia
- Ataxia can be caused by lesions outside the cerebellar cortex that involve cerebellar input or output pathways
- cerebellar peduncles, pons, corticopontine fibers, etc
Most common tests for appendicular ataxia
-finger -nose-singer and heel-shin test
Watch for dysmetria and dysrhythmia
Most common tests for truncal ataxia
- tandem gait (heel-to-toe gait)
- Patients will tend to fall or sway to the side of the lesion if it extends slightly into a cerebellar hemisphere, as with ischemia
- Romber test: note increased sway or fall
Cerebellar artery infarcts S/S:
-limb ataxia, unsteady gait, nystagmus, vertigo, N/V, HA
SCA cerebellar infarcts
- SCA and PICA most common
- ipsi ataxia with little/no brainstem signs
- mostly involves the cerebellum itself and usually spares the lateral brainstem
PICA cerebellar infarcts
-SCA and PICA most common
- ipsi atacis, with nystagmus, vertigo, and N/V
- involves inferior cerebellar peduncle and vestibular nuclei
-also can see signs of lateral medullary (Wallenberg’s) syndrome
AICA cerebellar infarcts
- supplies internal auditory artery
- unilateral hearing loss
What can mimic S/S of cerebellar infarcts?
-infarcts to lateral pons or medulla because of cerebellar peduncles and vestibular nuclei involvment
What happens if the cerebellum swells?
Can cause hydrocephalous because compression of the 4th ventricle. As well as compression of vital brainstem structures and subsequent herniation
Amyotrophic lateral sclerosis (ALS)
- lou Gehrig’s disease
- most common neuromuscular disease
- adult onset terminal disease of unknown cause
- characterized by the degeneration and scarring of neurons in the SC, brainstem (CST,CBT) and
- combination of both UMN and LMN resulting in limitation of movement
ALS etiology
- unknown, may be the result of multiple mechanisms that lead to neurodegeneration
- SODs-a group of enzymes that eliminate oxygen free radicals
- glutamate excitatory neuro transmitter can trigger a cascade of events leadingto cell death. inc levels in the CSF and plasma.
- clumping of neurofilament proteins
- lymphocytes are present which indicate immunoreactions
- environmental triggers
toxic theories for ALS
-related to lead or aluminum and abnormalities in magnesium and calcium levels
ALS pathophysiology
- massive loss of anterior horn cells of the SC and motor cranial nerve nuclei result in weakness and atrophy. greatest loss in Cervical and lumbar regions of the cord
- demyelination and gliosis of the CST and CBT
- Dementia
- reduce RNA in damaged cells
- accumulation of pigmented lipids
what is spared in patients with ALS?
- external ocular muscles III,IV,VI
- control of the muscles of the pelvic floor
- sensory systems and the spinocerebellar tracts are also generally spared
ALS diagnosis
- largely clinical
- criteria for diagnosis with EMG: spontaneous fibrillation and fasciculation in at least 3 limbs and the paraspinal muscles. these changes occur w/o any change in sensory response
- no single lab test but creatine phosphate levels are elevated in individuals with ALS
ALS clinical manifestation
-concomitant UMN and LMN sign in three spinal regions or two spinal regions with bulbar signs
-fasciculations: tongue, muscle crampls, stiffness, fatigue, weakness and atrophy.
hyper-refelxia, spasticity, positive Hoffman’s and babinski
Pseudobulbar palsy
-reflects damage in the corticobulbar tract
progressive bulbar palsy
- cranial nerve nuclei involvement
- weakness in the muscles that control chewing swallowing and facial gestures
- dysarthria
Primary lateral sclerosis
- result of neuronal loss in the cortex
- CST involvement including hyperactive reflexes, weakness, and spasticity
Progressive Spinal muscular atrophy
- loss of motor neurons in th anterior horn cells of the SC
- weakness and wasting in the muscles of the cervical spine, hands with progression to other are of the body including facial symptoms and respiratory failure
ALS treatment
-Riluzole: inhibits glutamate release. appears to be neuroprotective to slow the disease but it is not curative
-Celastrol: strong anti-inflammatory and antioxidant that suppresses nitric oxide production
-tamoxafin: inhibit PKC which mediates inflammation
talampanel minocycline, memantine, myotrophin, coenzyme Q10, ketogenic diet
Alzheimer’s dementia
- early in the disease coruse AD may have memory loss
- progressive aphasia or progressive apraxia
- decline in intellectual functioning severe enough tointerfere with personal relationships and an inability to carry out ADLs
Lewy Body disease
- progressive deterioration of cognition with no response to Parkinson’s medication
- presence of lewy bodies found in neurofibrillary tangle and senile plaques
-characterized by asymmetrical gait, apraxia, rigidity and myoclonus
Alzheimer’s : Pathology
- accumulation of insoluable material, amyloid. amyloid B protein is necessary t maintain fibroblasts and cell function. in AD the protein is not reabsorbed and tends to clump. when the clump contacts a neuron it destroys it
- loss of ACH and receptors
- glutaminergic neurons appear rpone to tangles
Alzheimer’s treatment
- no cure for AD
- treatment focuses on detection, early administration of cholinesterase inhibitors and/or NMDA receptor targeted therapy.
- dietary changes
Multiple sclerosis
- named for sclerotic plaques that develop on CNS
- multiple lesions are found throughout the brain and SC and slow or block neural transmission resulting in weakness, sensory loss, and visual disturbances
MS : etiology
- unknown, family history
- human leukocyte antigen region on chromosome 6 has been identified as the one genetic determinant for MS which contributes to a small fraction fro the genetic basis for MS
- coexisting autoimmune disorders are seen in a majority of MS patients
MS: pathophysiology
- chronic inflammatory autoimmune, demyelinating disease of the CNS
- an abnormality in the immune response that results in an attack on the individual own neural tissue
- may be triggered by virus or infectious agent
- Tcel mediated causingthe overproduction of proinflammatory cytokines that recruit inflammatory cells.
relapsing -remitting MS
-relapses with full recovery or some remaining neurological symptoms and residual deficits.
Primary -progressive MS
disease progression from the onset w/o remission
secondary- progressive MS
initial relapsing-remitting course followed by progression at a variable rate