Lesions And Diseases Flashcards

1
Q

Acute effects of thalamic syndrome

A

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)

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2
Q

Effects of chronic thalamic syndrome

A

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

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3
Q

Chorea cause

A

lesion in caudate nucleus [ GABA in connections of striatum to globus pallidus externa] GPe

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4
Q

Hemiballismus cause

A

Globus pallidus is inhibited.

lesion in subthalamic nucleus. ( decrease glutamate)

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5
Q

Athetosis cause
[Mobile spasm] No Fixed position / 🐍 dance

A

lesion of Globus pallidus. ( decrease GABA)
Defect in indirect pathway

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6
Q

Cause of pendular jerk

A

Cerebellum lesion

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7
Q

Hpotonia causes

A

Area 4 lesion

LMNL

Acute UMNL

  • Chorea (lesion in caudate)
  • Neocerebellar lesion

↑ Serum calcium

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8
Q

Spasticity

A

D.t Chronic UMNL
Type :
Clasp knife (initial resistance with sudden release)

-velocity dependent
- Hyperreflexia with no tremors
Clouns is present
- unilateral Circumduction gait

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9
Q

Rigidity

A

D.t : Parkinson
Type :
-Cog-wheal (interrupted)
-lead-pipe (continuous
-velocity independent
Static tremors disappear by voluntary movement

Shuffling Bilateral gait

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10
Q

Sensory ataxia

A

Site of lesion :Tabes Dorsalis

Romberg’s sign +Ve
Kinetic tremors : absent only at rest

Speech :Normal

Gait : Stamping (high)

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11
Q

Motor ataxia

A

Site of lesion : cerebrocerebellum

Kinetic tremors is present

Speech : staccato

Gait : zigzag

Nystagmus

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12
Q

Cause Gloves & stockings: patter of sensory loss.

A

Poly-neuropathy (peripheral neuritis)

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13
Q

Effects of syringomyelia

A

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

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14
Q

Most severe cases of syringomyelia

A

sensory effects
Motor effects
Automatic effects
Brain stem effects damage of cranial nerve nuclei (Syringobulbia)

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15
Q

Tabes dorsalis effects

A

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

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16
Q

Argyll- Robertson pupil

A

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)

-

17
Q

Effects of
Brown Sequard Syndrome = Hemisection of the spinal cord

A
  1. 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.
18
Q

Cause of Stage of spinal shock

A

sudden withdrawal of the supraspinal facilitatory impulses in cortico, reticulo & vestibule spinal tracts → prim Extra

↓ Excitability of spinal motor neurons & ↓Their responses to afferents.

19
Q

Effects of stage of spinal shock

A

-Loss of all reflexes
- loss Autonomic Defecation & micturition reflexes (retention)
- Muscle atrophy.
- Bone demineralization
- Vasomotor Sympathetic reflexes is lost→vasodilatation & hypotension

20
Q

Cause of recovery of reflexes

A

1) Denervation hypersensitivity of the remaining neurons →→ they can respond to afferents

2) collateral from existing neurons more stimulation of motor neurons & interneurons

21
Q

Manifestations of recovery stage

A

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

22
Q

+Ve Babinski sign

A

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

23
Q

Effects of LMNL

A

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.