Neuro Week 2 (B)

Front 1

Overall pathway (feedback loop) between the Cerebral Cortex to the Basal Ganglia?

Back 1

General act. of Cerebral Cortex
->Caudate Putamen
->Globus Pallidus +S.N. reticulata
->Thalmus (v.lateral+v.anterior)
->Back to cerebral Cortex (M-I)

Front 2

In this pathway, what is the "direct pathway"?

Back 2

Caudate Putamen
->GPSNR (inhibitory)
->Thalmus (v.l. +v.a.) (inhibitory)

Front 3

In this pathway, what is the "indirect pathway"?

Back 3

The projection back to the primary motor cortex, specifically the primary motor cortex (excitatory) (M-1)

Front 4

The _____ and _____ are essentially the same nucleus.

Back 4

Caudate and the putamen

Front 5

THe putamen recieves axons from what?

Back 5

The primary motor cortex and the primary sensory cortex.

Front 6

Another name for the cuadate putamen?

Back 6

The striatum

Front 7

Function of the Basal Ganglia?

Back 7

Serves as the repository of movement subroutines.

Front 8

What does the Basal Ganglia not do?

Back 8

It does NOT initiate movement or control evolving movement.

Front 9

What are subroutines?

Back 9

-Fragments of steriotypical movemnts.
-They are the output of the Basal Ganglia, directed at specific motor cortex for assembly into the final motor cortex pattern!

Front 10

What symptom in particular, characterizes Basal Ganglion Diseases?

Back 10

Involuntary Movements

Front 11

Examples of Hyperkinesia?

Back 11

-Chorea (dance like)
-Athetosis (stream of slow writhing movements)
-Balismus (violent movement)
-Tic

Front 12

Examples of Hypokinesia?

Back 12

-Bradykinesia (slow movement)

Front 13

Ballismus

Back 13

S: Violent moving in large amplitudes

C: Specific lesion to the subthalmic nucleus
-Ballistic movement to contralateral extremities

-T: Treat with dopamine antagonist

Front 14

Chorea

Back 14

S: involuntary dance-like movements, fragments of purposeful movements, easily disguised
-These are through whole body, whereas tics are associated with the head

Front 15

Huntington's Disease
-When does it start
-Signs
-Heriditary
-Cause

Back 15

-Typically 35-40
-Chorea and subcortical dimentia
-Autosomal Dominant
-Degeneration of Caudate nucleus

Front 16

Degeneration of Caudate nucleus causes what?

Back 16

The dis-inhibition of GPSNR

Front 17

Subcortical Dementia
-Signs

Back 17

-S:Personality changes, forgetfulness, depression, slowed thought process but NO language or mathmatics affected

Front 18

Subcortical Dementia
-Pathology

Back 18

-SLight cortical atrophy
-Striking basal ganglia atrophy (especially in cuadate and putamen)

Front 19

Cortical Dementia
-Signs

Back 19

-Severe sensory impairment, DECREASED language and mathmatical function
-Agnosia
-Apraxia

Front 20

Cortical Dementia
-Pathology

Back 20

-Striking cortical atrophy
-Little basal ganglia atrophy

Front 21

What is Agnosia?

Back 21

Inability to attach meaning to various sensory stimuli

Front 22

What is apraxia?

Back 22

Inability to preform motor tasks without impairment of motor or sensory systems

Front 23

Huntington disease
-genetics
-#'s

Back 23

-Autosomal Dominant
-CAG repeat
-Average: 19
-Disease expression: >34

Front 24

Is a mutation for huntington's disease more likely during oogenesis or spermatogenesis?

Back 24

Mutation is more likely during spermatogenesis

Front 25

What is the cause of Huntingtons disease?

Back 25

-CAG codes for glutamine, polyglutamines interfere with intracellular transport

Front 26

Wilsons diseaase
-AKA
-Cause

Back 26

-AKA: Hepatolenticular degeneration
-It is a defects in coppor metabolism

Front 27

What are the three manifestations of Wilsons disease?

Back 27

-Hepatic
-Psychiatric (psychosis or depression)
-Neurologic

Front 28

Neurologic side effects of wilsons disease?

Back 28

-Chorea
-Myoclonus (muscle twitching)
-Dystonia
-Tremor
-Bradykinesia

Front 29

What is the type of disorders from Wilsons disease?

Back 29

Psychiatric + Basal ganglion movement disorders

Front 30

What excess is not excreted in Wilsons disease?

Back 30

Greater than 0.25mg/day of Copper.

Front 31

Locations of Cu accumulation in Wilson's disease?

Back 31

-Brain
-Eyes (Kayser-Fleisher!!)
-Kidneys (a key sign)
-Liver

Front 32

What is the treatment for Wilson's disease.

Back 32

Cu chleating agents (penicillamine first)

Front 33

Tremor
-Characterized by

Back 33

-Involuntry!
-Rhythmic oscillation by reciprocally innervated muscles

Front 34

Essential Tremor

Back 34

-May include any extremity
-Long standing (3-5 years)
-Usually familial

Front 35

Essential tremor treatment

Back 35

-Deep brain stem stimulation can be extremely efective

Front 36

Dystonia

Back 36

Involuntary slow muscle contractions causing a twisting of the body (leads to contorsions)

Front 37

What is maintained in Dystonia?

Back 37

Strength and sensation

Front 38

4 Types of Dystonia?

Back 38

-Generalized
-Segmantal
-Focal (writers cramp)
-Unilateral (hemidystonia)
-usually due to a lesion in the contralateral striatum

Front 39

Dystonia Muscularis deformans

Back 39

-Inherited, childhood onset
-codes for ATP binding protein TORSIN A
-Generalized Dystonia

Front 40

Dopa Responsive Dystonia
-Treatment

Back 40

-Often mistaken as DMD
-Daily changes that worsen in the afternoon

Front 41

Parkinsons
-Symptoms
-Tremor rate

Back 41

-Bradykinesia (slowed voluntary movement, diff stop and start)
-Rigidity (Lead pipe and cog wheel)
-4-7 htz pill rolling

Front 42

Parkinsons Pathology
-Cause

Back 42

-Loss of dopamine producing cells in S.N. Pars Compacta
-Formation of Lewy bodies

Front 43

Parkinsons disease cause

Back 43

-Toxic ROS's (toxic to CNS that is)

Front 44

What loop s lost with Parkinsons?

Back 44

Feedback loop between cerebral cortex and the basal ganglion

Front 45

Parkinsons treatment

Back 45

-L-Dopa + caradopa (inhibits conversions of LDOPA to DA before BBB)

Front 46

When to use Ldopa?

Back 46

-After you have exhauseted all other efforts (due to Dopa desensitization)

Front 47

Progressive Supranuclear Palsy

Back 47

-Parkinsons + eye movement disorder

Front 48

Multisystem atrophy

Back 48

Parkinsons Bradykinesia WITHOUT tremor!!!
-Autonomic dysfunction
-Ataxia

Front 49

Normal Pressure Hydrocephalus

Back 49

Parkinsons Bradykinesia + mental slowing+ urinary incontinance

Front 50

Olivopontocerebellar atrophy

Back 50

Parkinsons+Ataxia+dysarthria (speech)

Front 51

What does and doesent the cerebellum do?

Back 51

-Doesnt:
-no initiate movement
-not a repository for stereotypical movements
-Does:
-Acts only on evolving movement
-REgulates timing of individual motor unit contracts

Front 52

What are the imputs of the cerebellum?

Back 52

-Mossy fibers (to cerebellar cortex)
-CLimbing fibers (to purkinje cell)

Front 53

What are the outpus of the cerebellum?

Back 53

-From Cortex-Purkinje Cell
-From deep nuclei
-Fastigial
-Globose/interpositis
-Dentate (most prominent)

Front 54

Are climbing fibers inhibitory or excitatory to the parallel fibers?

Back 54

Excitatory

Front 55

Are basket cells inhibitory or excitatory to the parallel fibers?

Back 55

Inhibitory

Front 56

What are the three functional zones of the Cerebellum?

Back 56

-Vestibulocerebellum
-Spinocerebellum
-Cerebrocerebellar

Front 57

Vestibuloceribellar

Back 57

-Flocular lobe and nodular lobe
-the little ones at the bottom
-Connected to the vestibular system

Front 58

Spinocerebellum

Back 58

-Vermis + intermediate zone
-Connected to the spinal cord

Front 59

Cerebrocerebellum

Back 59

-Hemispheres
-connected to the cerebral cortex via the deep pontine nuclei