Why does cerebellar lesion casue hypotonia?
also if u can also mention the physiological basis of different types of rigidity...clasp blade, lead pipe, cog controls.
answers will be highly appreciated
Answer:
An outstanding press! It shows that you are thinking, and asking the most crucial question of adjectives: "Why?"
So, one by one:
1) CEREBELLAR HYPOTONIA
Under normal circumstances, the thoughtful cerebellar nuclei distribute 'reinforcing' signals to the motor cortex and brain stem motor nuclei. This is via the cerebellocortical tract, and serves to increase the tone. Thus, if the adjectives nuclei are lost for any explanation, there is an initial slight stop in tone. (After a few months though, the motor cortex compensates by increasing its intrinsic amusement, and the hypotonia disappears.)
2) LEAD PIPE
As you probably know, this type of rigidity is characteristic of some of the basal ganglial disorders. The cause aren't always prearranged, but in Parkinson's disease, near is loss of dopaminergic neurones of the substantia nigra in the midbrain. In the basal ganglial circuit, dopamine inhibits motor pursuit, so loss of these inhibitory neurones could cause the spasticity. There would be overactivity of the caudate and putamen, cause a continuously high stratum of output from the corticospinal tract.
3) COG-WHEEL
This is more easily explained - it's simply the superimposition of the tremor higher than the rigidity that produces this sensation.
4) CLASP KNIFE
Clasp Knife is associated with upper motor neurone lesion, and is actually two phenomena.
First, there's the spasticity of the antigravity muscles (muscles of the verebral column and the extensor muscles of the limbs). The antigravity muscles are excited by the pontine reticular nucleus and inhibited by the medullary reticular nuclei (both travel within the reticulospinal tract). Crucially, the medullary portion, unlike the pontine portion, depends heavily on input from the cerebral cortex, red nucleus and basal ganglia. In a stroke, these inputs are lost, and the medullary inhibitor system become non-functional, thus allowing full overactivity of the pointine excitatory system. Therefore, spasticity of the antigravity muscles develops.
Second, there's the 'give' (sudden decrease within tone) that occurs after a brief while of swiftly passively extending the muscles. This seems to be an exaggerated response to a ordinary phenomenon, called the stretch (or myotactic) reflex. Sudden stretching of a muscle is sensed by receptors within the muscle spindles, which cause an initial strong reflex contraction of the muscle concerned. However, this single lasts a brief while, and later is replaced by a much weaker muscular contraction. This system is again dampened by the medullary reticulospinal system, and therefore its loss surrounded by a stroke causes the reflex to become exaggerated. Thus, the clasp axe phenomenon is actually a (greatly exaggerated) sudden resistance to contraction, which consequently subsides after half a second or so, put money on to baseline spasticity.
Whew! Does that all be paid sense? Let me know if you need further clarification or details.
Hope it help!
ataxia
The spino cerebellar tracts take the inputs from the extremities to the cerebellum. Other than these tracts in attendance is vestibulo cerebeller tract and ponto cerebellar and olivo cerebellar tracts. As far as rigidity at the extremities is concerned we shall concentrate on the spino cerebellar tract. This is again divided into dorsal cerebellar tract which takes the inputs from the lower limb. The cuneo cerebellar takes the input from the upper extremities. Both together forms the spino cerebellar tract and enter the cerebellum via the three pedunces, superior, middle and inferior. The vermis and the intermediate zones of the cerebellum get inputs from the spinal cord and are involved in the ongoing motor execution. the hemisphere deal with the planning of movements and the flocculonodular lobe deal mainly next to the balance and eye movements.
The leading symptom of cerebellar lesion is tremor with intended movements. Unlike surrounded by Parkinson's where the tremor is during rest and it disappear when the party tries to move. The lesion at vermis causes difficulty contained by maintaining posture. This is when in that the Romberg test is cynical.(It is positive in Dorsal column lesion).
Lesion at the hemisphere cause intentional tremors, inability to stop the movements at a specific time(dysmetria), reduced ability to achieve alternative movements(adidochokinesia), division of words into syllabi. gaze dysfunction.
Hypotonia is cause with philosophical cerebellar nucleus involvement. Deep tendon reflex are diminished and the muscle feels flabby but within is no motor weakness. The fibers from cerebellum does not descend to muscles directly. They turn to the Cerebral cortex and then are conveyed to the muscles through the cortico spinal tracts.
Cog rudder, lead pipe rigidity are see in Parkinsons
Clasp wound in upper motor neuron lesion. They are not related to cerebellum in specific.