1. Extrapyramidal system and Cerebellum

2. Extrapyramidal system consists of:
cortical areas 4, 6, 8
the basal ganglia: n. caudatus, n.lenticularis (putamen, globus palidus)
the nuclei of brain stem (black substance, red nucleus, vestibular nuclei, reticular nuclei, nucleus of Darkshevych, Lues’ body, lower olives)
spinal cord: -motor neurons and -small motor neurons, which are located in anterior horns of the spinal cord

3. Two parts of Extrapyramidal system:
Pallidum
globus palidus
black substance
red nuclei
vestibular nuclei
nucleus of Darkshevych
lower olives
Lues body
Pallidum is phylogenetically older then striatum. That’s why in newborn babies pallidum dominates

4. Two parts of Extrapyramidal system:
Striatum
cortical areas 4,6,8
n. Caudatus
Putamen
Only at the age of 4 – 5 months old striatum starts to influence on motor functions

6. Connections of Extrapyramidal system:
Pallidum and striatum are closely connected with each other by means of such pathways:
nigrostriatal (dopaminergic) – black substance – nucleus caudated – it inhibits the neurons of striatum
strionigral (GABA-ergic)- nucleus caudated (GABA) – black substance – it controls production of dopamine.

7. The afferent pathways of Extrapyramidal system:
T – EPNS – T
T – cortex – EPNS – T
T – cortex - pons – cerebellum – thalamus
The efferent pathways of Extrapyramidal system:
Tr. olivospinalis
Tr. rubrospinalis
Tr. vestibulospinalis
Tr. tectospinalis
Tr. reticulospinalis

8. Functions of Extrapyramidal system
It prepares muscles to smooth economical movements
It determines the posture
It makes automatical involuntary regulation of active conscious movements
It provides automatical stereotyped movements and reflector protective movements
It provides motor manifestation of emotions

9. Extrapyramidal system’s lesion:
Parkinson’s syndrome (lesion of pallidum)
Syndrome of involuntary movements (lesion of striatum)

10. Parkinson’s disease
In 1817 – James Parkinson described the major manifestation of this syndrome
In 1874 – this disease was called after James Parkinson – Parkinson’s disease
In 1920 – Tretiakov noticed that the greater cell loss in substantia nigra, the lower concentration of dopamine is in striatum and more severe the degree of clinical Parkinsonism.

11. E t i o l o g y
According the modern investigations in base of this disease is inborn dificiency of tyrosintransferase enzyme in dopamine.
Parkinsonism may be defined in biochemical term as an inborn dopamine deficiency state.

12. Basic symptoms of Parkinson’s syndrome:
Hypokinesia (Akinesia)
Rigidity
Tremor

13. The main pathogenetic mechanisms:
Great cell loss in the substantia nigra, low concentration of dopamine in striatum, the influence of striatum on pallidum. As a result akinesia occurs.
The main cause of rigidity is increasing of tonic reflex on muscles tension.
The main source of tremor is thalamus ( its nucleus ventrolateralis ).

14. Hypokinesia (Akinesia)
Bradykinetic and akinetic state
The gait is shuffling and the steps are slight
Parallel footprints
The loss of associated swinging of the arm or arms when walking - (acheirokynesis)
A lack of mobility of facial expression (Bechterev’s symptome)
Infrequent blinking of the eyelids (Mary’ s symptome)
Fixed look

15. Hypokinesia (Akinesia)
Inertia of rest (that means it is very difficult for patient to start moving)
Inertia of movement (the so-called propulsive gait, lateropusion or retropulsion)
Micrography – handwriting is too small
Speach is quite and inexpressive (bradylalia)
Paradoxical kynesia is possible after strong impression or great emotions

16. plastic type of increased muscle tone:
Rigidity
plastic type of increased muscle tone:
Cogged-wheel symptom (in carporadial joint)
Tonus increases in course of evaluation of nervous system state
Tonus is expressed in the same manner in the group of flexors and extensors

17. Tremor:
Are much more expressed in distal parts of extremities, sometimes tremor of lips or lower jaw can occur
It looks like coins counting
It is much more expressed while resting. It disappears or decreases while moving
Its frequency is 3 – 6 times per second

18. Other features of Parkinson’s disease
Bradyphrenia (thoughts are too slow)
Bradymnesia (recollection is slow too)
While speaking such patients are boring (akairia - Astwatsaturov symptome)
Usually they are in a bad mood. Depression is very typical for the patients with Parkinson disease
Sometimes they have autonomic disorders
Parasympathetic nervous system dominates in such patients – they have running saliva (aeriel symptome), hyperhydrosis, fatty skin and type of hair, bradicardia and arterial hypotension

19. The symptom of air pillow or Vartenberg symptom –
T e s t s:
The symptom of air pillow or Vartenberg symptom –
The patient is lying down. One props up his head a little bit and then quickly takes his hand out. Normally the head is falling down. But in patients with Parkinson disease the head stays in the same position for a while.

20. T e s t s:
Westfahl’s phenomena of paradoxical muscle constriction – While foot extension it stays in the same position for a while.
Hand extension test.
Test of knee flexion – The patient is lying on his abdomen; his lower extremities are bended in knees. In patients with Parkinson disease the legs are fixed in this position for several minutes.

21. The symptom of Noica–Haneva Tests:
While evaluations of muscle tone one asks the patient to raise his opposite extremity. In patients with Parkinson disease the tonus suddenly increases.

22. Clinical forms of Parkinson disease:
Rigid (hypokynesia dominates)
Trembling
Mixed :
rigid – trembling or trembling – rigid

23. The degree of severity (according to Petelin):
The first degree - expressed one or two main symptoms. The patient preserves professional and home activity
The second degree – The patient is disabled professionally
The third degree – The patient cannot take care of himself

24. Symptomatic Parkinsonism
Craniocerebral trauma ( Muhammad Ally)
CO, Mn intoxication
Brain tumor
Encephalitis (Economo)
Strokes
Cerebral atherosclerosis
Medicinal parkinsonism (reserpinum, neuroleptics)
Poisoning of heavy metals

27. Hyperkynetic–hypotonic syndrome:
The main clinical signs of this syndrome are:
Muscular hypotonia
Involuntary movements – hyperkynesis.
Involuntary movements are characterized by:
the amplitude of the movement
location of muscle involved
the rate
the duration of contraction and the relaxation

28. Kinds of hyperkynesis Chorea Athetosis Choreoathetosis
Ballism and hemiballism
Myoclonus
Torsion spasm
Tics
Facial cramp
Tremor

29. C h o r e a
spontaneous, irregular, purposeless and asymmetric movements
they are present at rest and subside during sleep
eyes and tongue symptom ( or Hersonsky’s symptom ) - the patients are unable to maintain tongue protrusion for more than a few seconds;
Hordon’s II symptom – while checking knee – reflex crus stays in the position of extension for a while and then slowly goes down;
Cherni symptom - pathologic sudden abdomen at breath.
The most common diseases - Huntington’s chorea (inherited disease), rheumatic subcortical encephalitis or chorea Sydenhams (juvenile disease), atherosclerotic chorea, chorea gravidarum, electric chorea.

30. A t h e t o s i s
Movements are slower and more sustained than choreiform movements
they affect primarily the distal portion of extremities
snakelike movement of any combination of flexion, extension, adduction and abduction in varying degrees
They are regularly associated with increased muscular tone
It is supposed that athetosis is the result of nucleus caudated lesion.
Choreoathetosis
is a term selected to describe movements that are intermediate between chorea and athetosis.

31. Ballism and hemiballism
Its the more or less continues gross abrupt contractions of axial and proximal muscles of the extremities
In the most cases this movement disorder is confined to one side of the body (hemiballism)
It may be associated with hypotonia

32. Torsion spasm Twisting or turning movements
The muscles of trunk and neck are involved
Sometimes torticollis can occur
Usually it is the result of putamen lesion

33. Myoclonus
Is a jerking movement of one or more muscle groups (for example palatine, tongue, pharynx, larynx, diaphragm and skeletal muscles)
Usually only one muscle group is involved
They are synchronous in most of cases and sometimes they are asynchronous
Their frequency is about 15 – 18 per minute
They may be induced by visual, tactile, or auditory stimuli (stimulus-sensitive myoclonus) or by the initiation of the voluntary movement (intention myoclonus).

34. T i c s are an involuntary compulsive stereotyped movements
they may be simple or complex
tics may involve any portion of the body ( they are most common about the face where they are manifest as blinking, grinning, smirking, lip licking, nose wrinkling)
Facial cramp
is tonic seizure in facial muscles
Tremor
Is rhythmical jerking of arms, legs or head
Its frequency is about 4 – 6 per second

38. C e r e b e l l u m
is a reflexional organ of coordination of movements, equilibrium and muscular tone

39. C e r e b e l l u m Two large lateral hemispheres
Contains :
Two large lateral hemispheres
Flocculo-nodular lobe (vermix)
Three pairs of peduncles.

40. Grey matter of cerebellum
Is presented by cortex of hemispheres and nuclei of cerebellum:
Nucleus fastigii
Nucleus globosus
Nucleus emboliformis
Nucleus dentatus

41. Cerebellum peduncles:
The lower peduncles (corpora restiformia) provide connection with oblong brain and spinal cord:
Tr. spinocerebellaris dorsalis (Flexig’s)
Tr. vestibulocohlearis (from nuclei vestibularis to nucleus fastigii)
Tr. olivocerebelaris (from lower olives to nucleus dentatus)
Fibre arcuate externe (from nuclei Holl and Burdach to hemispheres and vermis)

42. Cerebellum peduncles:
The middle peduncles (pedunculum cerebellaris medii) provide connection with pons
Tr. pontocerebellaris. They connect nuclei of pons with the opposite hemisphere of cerebellum

43. Cerebellum peduncles:
The upper peduncles of cerebellum (pedunculi cerebellaris superior) connect cerebellum with middle brain. They include two systems:
Afferent one – from spinal cord to cerebellum – tr. spinocerebellaris ventralis (Hover’s)
Efferent one – from cerebellum to the structures of extrapyramidal nervous system – tr. cerebellotegmentalis et tr. dentorubralis.

44. The way of cerebellum correction
The first neuron – tr. fronto-temporo – occipito- pontinus
The second neuron – tr. pontocerebellaris (pontino- cerebellaris decussation)
The third neuron – tr. cerebello – dentatus
The forth neuron – tr. dentorubralis (Vernekink’s decussation)
The fifth neuron – tr. rubrospinalis (Forel’s decussation)
The sixth neuron – tr. spinomuscularis

46. The main functions of cerebellum:
body equilibrium
regulation of muscle tone
coordination of movements
synergy

47. Hemispheres function are:
Vermix function are:
Equilibrium of the body
Regulation of muscle tone
Hemispheres function are:
Coordination of the movements of extremities
Synergy of the muscle

48. A t a x i a
means disturbances of equilibrium of the body and coordination of movements.
Cerebellum lesion produces cerebellar ataxia:
Static (lesion of vermix)
Dynamic (lesion of hemispheres)

49. Kinds of ataxias: Cerebellar (cerebellum lesion)
Sensitive (loss of deep joint sense)
Frontal (cortical) (lesion of Frontal lobe)
Vestibular (lesion of vestibular apparatus)
Hysterical (in case of Hysteria)
Mixed

50. Cerebellar ataxia Attactic gait – patient can’t to walk
Disorders of equlibrium – patient can’t to stand
Muscular hypotonia
Intention tremor – is dynamic tremor (it is more expressed while moving and disappears while rest)
Nystagmus: horizontal, vertical, vertical rotary, or dissociated (different in each eye)
Scanning speech –patient can’t to speak slowly
Macrographia – handwriting is too large
Dysmetria (disturbed ability to gauge distances)
Adiadochokinesia (disturbed ability to perform rapid alternating movements)
Asynergia – disturbed ability to controls function of antagonists muscles

51. Symptoms of lesion Cerebellar lower peduncles lesion can cause:
Cerebellar ataxia
Bulbar syndrome
Sometimes pathology of Holl’s and Burdach’s nuclei is associated with this lesion. Then ataxia is complex and is called cerebellar – sensitive ataxia.
Cerebellar upper peduncles lesion can cause:
Cerebellar ataxia at the side of lesion
Trochlear Nerve lesion
Midbrain lesion symptoms

52. Symptoms of lesion Nucleus ruber lesion can cause:
Cerebellar ataxia in the opposite extremities
Resting tremor
Webber’s syndrome or paresis of convergence may occur
Pontino – cerebellar angle lesion manifests as:
Cerebellar disorders and pathology of VII, VIII, V, VI pairs of CNs at the side of lesion
Pyramidal and sensory hemisyndrome on the opposite side