Lesions And Diseases Flashcards
Acute effects of thalamic syndrome
1) Acute (immediate) Mention:
a) Crossed (contralateral) hemianesthesia, loss of all sensations on the opposite side of body & face
b) 2ry hyperalgesia due to release from gate inhibitory fibers
c) Sensory ataxia (+Ve Romberg)
Effects of chronic thalamic syndrome
a) Recovery of crude sensation only
The recovered sensations are:
Need high threshold stimulation Poorly localized
b) 2ry hyperalgesia
c) Attacks of pain
Thalamic hyperpathia (unpleasant sensation)
e) Emotional disturbances
f) Motor ataxia
Chorea cause
lesion in caudate nucleus [ GABA in connections of striatum to globus pallidus externa] GPe
Hemiballismus cause
Globus pallidus is inhibited.
lesion in subthalamic nucleus. ( decrease glutamate)
Athetosis cause
[Mobile spasm] No Fixed position / 🐍 dance
lesion of Globus pallidus. ( decrease GABA)
Defect in indirect pathway
Cause of pendular jerk
Cerebellum lesion
Hpotonia causes
Area 4 lesion
LMNL
Acute UMNL
- Chorea (lesion in caudate)
- Neocerebellar lesion
↑ Serum calcium
Spasticity
D.t Chronic UMNL
Type :
Clasp knife (initial resistance with sudden release)
-velocity dependent
- Hyperreflexia with no tremors
Clouns is present
- unilateral Circumduction gait
Rigidity
D.t : Parkinson
Type :
-Cog-wheal (interrupted)
-lead-pipe (continuous
-velocity independent
Static tremors disappear by voluntary movement
Shuffling Bilateral gait
Sensory ataxia
Site of lesion :Tabes Dorsalis
Romberg’s sign +Ve
Kinetic tremors : absent only at rest
Speech :Normal
Gait : Stamping (high)
Motor ataxia
Site of lesion : cerebrocerebellum
Kinetic tremors is present
Speech : staccato
Gait : zigzag
Nystagmus
Cause Gloves & stockings: patter of sensory loss.
Poly-neuropathy (peripheral neuritis)
Effects of syringomyelia
1- Damage of spinothalamic fibers of both sides → loss of pain & temperature on both sides at the level of the lesion → jacket distribution of sensory loss.
2- Crude touch is not lost because it is partially carried by the dorsal column
Most severe cases of syringomyelia
sensory effects
Motor effects
Automatic effects
Brain stem effects damage of cranial nerve nuclei (Syringobulbia)
Tabes dorsalis effects
Early stage:
Inflammation irritation of pain →» fibers → severe attacks of L.L pain.
Late stage:→ all spinal Formation of syphilitic gumma → compression & destruction of nerves
Argyll- Robertson pupil
Loss of pupillary light reflex but the pupil itself is normal & can respond to other reflexes such as the near response
In more severe stages of tabes dorsalis
Due to Damage of pretectal area (center of pupillary light reflex, in mid brain)
-
Effects of
Brown Sequard Syndrome = Hemisection of the spinal cord
- At the level of the lesion:
On the same side of lesion: -
*Sensory: loss of all sensations at corresponding dermatome.
- Motor: lower motor neuron lesion (LMNL) = flaccid paralysis = no reflexes.
2- Below the level of the lesion:-
Same side:
Loss of proprioception. *Sensory: loss of D.C. sensations
*Motor: upper motor neuron lesion (UMNL)
= spastic paralysis = ↑ reflexes.
Opposite side:
- Sensory: loss of spinothalamic sensations.
Cause of Stage of spinal shock
sudden withdrawal of the supraspinal facilitatory impulses in cortico, reticulo & vestibule spinal tracts → prim Extra
↓ Excitability of spinal motor neurons & ↓Their responses to afferents.
Effects of stage of spinal shock
-Loss of all reflexes
- loss Autonomic Defecation & micturition reflexes (retention)
- Muscle atrophy.
- Bone demineralization
- Vasomotor Sympathetic reflexes is lost→vasodilatation & hypotension
Cause of recovery of reflexes
1) Denervation hypersensitivity of the remaining neurons →→ they can respond to afferents
2) collateral from existing neurons more stimulation of motor neurons & interneurons
Manifestations of recovery stage
1) Return of reflex the latest is knee and ankle jerks
2) Sexual reflexes:
The cortical complex sexual desire & act is lost,
3) micturition Return but without voluntary control (as infants) Filling of 150 mL urine reflex evacuation of bladder (automatic bladder)
4)Return of infantile reflexes:
Grasp reflex
+ve Babiniski
5)Mass reflex
Flexion of both L.L.
Contraction of abdominal muscles
Evacuation of bladder & rectum
Increase ABP
Erection
Sweating below level of lesion
After scratching skin of L.L. or abdominal wall
+Ve Babinski sign
1) Lesion in premotor area 6 ( fanning of 4 lateral toes )
2) Lesion of primary motor area 4 (dorsiflexion of big toe)
3) Recovery stage after spinal shock
4) UMNL
Effects of LMNL
1) Ipsilateral, localized flaccid paralysis of a muscle or group of muscles supplied by the affected nerve.
The paralyzed muscle may show:
- Fasciculations: Felt & seen
jerky contraction of a group of muscle fibers
Due to pathological discharge of A.Ch from the damaged motor neuron.
- Fibrillations: Felt & not seen
contraction of an individual fiber
Due to denervation hypersensitivity.
