Basal ganglia


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Dr T Ravikanth, svs medical college, ap psychiatry

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Basal ganglia

  1. 1. BASAL GANGLIA Presenter : Dr. T. Ravikanth Moderator : Dr. V. Sharbandh Raj
  2. 2. OUTLINE• Overview of Basal Ganglia structure• Basal Ganglia – components and connections 1. The caudate nucleus, 2. The putamen, 3. The globus pallidus (referred to as the paleostriatum or pallidum), 4. The subthalamic nucleus, 5. The substantia nigra• Neural circuits of the Basal Ganglia• Modulation of inputs and outputs to the Basal Ganglia• Summary of extrapyramidal circuitry• Functional considerations
  3. 3. Basal Ganglia System• The basal ganglia are a collection of nuclei that have been grouped together on the basis of their interconnections.• These nuclei play an important role in regulating movement• Role in certain disorders of movement (dyskinesias), which include – jerky movements (chorea), – writhing movements (athetosis), – rhythmic movements (tremors). –• In addition, more recent studies have shown that certain components of the basal ganglia play an important role in many cognitive functions.• Derived from telencephalon and partly diencephalon
  4. 4. BASAL GANGLIA• The basal ganglia are generally considered to include 1. The caudate nucleus, 2. The putamen, 3. The globus pallidus (referred to as the paleostriatum or pallidum), 4. The subthalamic nucleus, 5. The substantia nigra
  5. 5. Basal ganglia structuresThis cartoon represents a horizontal slice through the brain at the level of the thalamus.It is a midline view from above, with anterior at the top of the screen and posterior atthe bottom of the screen.5
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  8. 8. 8 Basal Ganglia menu
  10. 10. Caudate nucleus and putamen are continuous rostroventrally, beneath the anterior limbof internal capsule and dorsal regions where slender grey cellular bridges pass across the posterior limb of IC.
  11. 11. Striatum• Electron microscope indicate the striatal neurons fall into 2 categories:1. Spiny dendrites : mc – Large nucleus with 7-8 pri. dendrites covered with spiny processes • Type I – axons reach GP/S.Nigra ; NT : GABA, Leutenkephalin • Type II – stubby and less dense spiny processes ; NT - ??Substance P2. Smooth dendrites – small varicose and recurring dendrites and short axon , no spiny processes – NT : GABA
  12. 12. Caudate Nucleus• The caudate nucleus is a C-shaped structure that is divided into three general regions. 1. Head 2. Body 3. Tail• The caudate nucleus is associated with the contour of the lateral ventricles: the head lies against the frontal horn of the lateral ventricle, and the tail lies against the temporal horn.• The head = continuous with the putamen• The tail = terminates in the amygdala
  13. 13. Putamen• The putamen lies in the brain – medial to the insula – bounded laterally by the external capsule – medially by the globus pallidus.• As noted earlier, the putamen is continuous with the head of the caudate nucleus.• Although bridges of neurons between the caudate nucleus and the putamen show the continuity of the nuclei, the two structures are separated by fibers of the anterior limb of the internal capsule.
  14. 14. STRIATAL CONNECTIONS• Afferent connections from1. Cerebral cortex2. Amygdala3. Thalamus4. Substantia nigra5. Dorsal nucleus of Raphe
  15. 15. Striatal connections (afferent)1. Cortico striate fibresi. Primary motor area B/L Putamenii. Premotor area I/L CN and Putameniii. Prefrontal cortex CN• NT : Glutamate2. Amygdalo striate fibres• Part of limbic sytem = behaviour
  16. 16. Striatal connections (afferents)3. Thalamostriate fibres – Intra laminar thalamic Nu. to Striatum4. Nigro striatal fibres – Pars compacta of S.nigra to striatum – NT : Dopamine5. Dorsal Nu. Of Raphe(Mesencephalon) – Project to striatum ; inhibitory – NT : 5 HT
  17. 17. Striatal connections (efferent)• Effrent fibres to GP and S.Nigra1. Striato pallidal fibres: – CN – IC – GP & SN – Putamen – medially – GP & SN – NT : GABA2. Striato Nigral fibres : – Project on pars reticulata – NT : GABA & Enkephelin (spiny 1), substance P(spiny2)
  18. 18. Globus Pallidus• globus pallidus is derived from the diencephalon.• lentiform nucleus = forms a cone-like structure, with its tip directed medially.• The posterior limb of the internal capsule• putamen• medial medullary lamina
  19. 19. PALLIDAL CONNECTIONS• Pallidal afferent fibres: – From : Striatum and STN (Sub thalamic Nu.) – Unlike striatum : not from c.c, thalamus,s.n1. Striopallidal fibres : – NT : GABA(M&L) > enkephalin(L)> substance P(M) – Patients with Huntington’s disease have low levels of NT in GP2. Subthalamopallidal fibres : – NT : GABA – Inhibitory action on pallidum via interneurons
  20. 20. Pallidal connections (efferent)• Pallidofugal fibres to different brain stem Nu.• Medial pallidal seg. – Thalamic Nu., mid brain RF & S.Nigra – Pallidothalamic fibres to ventral anterior and ventro lateral thalamic nuclei• Lateral pallidal seg. – Subthalamic Nu & S.Nigra – Pallido subthalamic projections are inhibitory to STN via GABA.• Pallido Nigral fibres terminate preferentially upon dopaminergic neurons in pars compacta (unlike striatonigral fibres on pars reticulata) via GABA & substance P
  21. 21. Subthalamic Nucleus• The subthalamic nucleus (of Luys) is also derived from the diencephalon.• The large-celled nucleus lies – Dorsomedial to the posterior limb of the internal capsule – Dorsal to the substantia nigra – Ventral to thalamus – Lateral and caudal to hypothalamusDiscrete lesions of thesubthalamic nucleus in humanslead to hemiballism, a syndromecharacterized by violent, forcefulchoreiform movements thatoccur on the side contralateral tothe lesion and inv. primarily prox.muscles.
  22. 22. Subthalamic connections• Afferents : – Motor, premotor and prefrontal cortex – Thalamus – Lateral pallidal segment (major) – Pedunculopontine nucleus• Efferent projections: – Both segments of GP (M&L) – Substantia Nigra
  23. 23. Substantia Nigra• The substantia nigra is present – in the midbrain – between the tegmentum and the basis pedunculi – mesencephalic in origin – Highest concentration of GABA in CNS• The substantia nigra consists of two components: – Pars compacta : dorsal cell–rich portion • Pigmented(neuromelanin) neurons = contain Dopamine • Principal source of striatal dopamine – Pars reticulata : ventral cell–sparse portion • Inhibitory neurotransmitter GABA.
  24. 24. Substantia nigra - connections• Afferents from : 1. Striatum 2. GP 3. STN 4. Dorsal Nu. Of Raphe 5. Pedunculopontine Nu. 6. Nucleus accumbens• Efferents fibres from SN broadly classified as : A. Dopaminergic A. Pars compacta to striatum and Dorsal nu. of Raphe B. Non – Dopaminergic A. pars reticulata to thalamus, tectum, tegmentum
  25. 25. Input OutputSubstantia nigra Striatum Striatum (from pars Pallidum compacta – DA) STN, PPN, DNR.Subthalamic Nucleus Lateral pallidal segment, Globus pallidus Motor cortex Pars reticulata (S.N)
  26. 26. Neural circuits of the Basal Ganglia
  27. 27. Neural circuits of the Basal Ganglia circuitry The basal ganglia form an internal motor circuit … Cortex Caudate Putamen 31
  28. 28. The cortex receives motor planning information, then passes that information to the caudate & putamen, which govern timing of events32
  29. 29. The information then is passed to the globus pallidus …33
  30. 30. ... which helps govern movement magnitude, and then passes this basal ganglia output to thalamus nuclei34
  31. 31. Modulation of input to the Basal Ganglia
  32. 32. Modulation of input to the Basal Ganglia The caudate & putamen Input modulation receive input from the cortex, and … 36
  33. 33. … from the thalamus.37
  34. 34. The substantia nigra also modulates input to the basal ganglia.38
  35. 35. Reciprocal connections with the caudate & putamen allow exitatory inputs from the substantia nigra to modulate the amount and type of output sent to the globus pallidus. Dopamine is the neurotransmitter used by these substantia nigra pathways.39
  36. 36. When the substantia nigra isn’t working properly, input to the basal ganglia isn’t modulated properly, and the globus pallidus receive progressvely less information. Without this information, the initiation of movement (i.e., timing) message is less effective and the person’s movements progressively become slower (i.e., bradykinesia).40
  37. 37. Parkinson’s disease is related to a deterioration of the substantia nigra and globus pallidus, and is characterized by resting tremors and bradykinesia.41 Basal Ganglia menu
  38. 38. Modulation of output from the Basal Ganglia
  39. 39. Modulation of output from the Basal Ganglia Output modulation - part 1 1) The putamen provides processed information to the globus pallidus.
  40. 40. - part 1In addition to modulatinginput to the basal ganglia,the substantia nigra alsomodulates the output.
  41. 41. - part 1The substantia nigra, in turn, hasmany connections.
  42. 42. - part 22) The subthalamus plays a role in modulating output from the basal ganglia
  43. 43. - part 2Deterioration of thesubthalamus results in theballisms, or explosivemovements occurringperiodically, thatcharacterize Huntington’sdisease.
  44. 44. Neural circuits of the Basal Ganglia - A summary
  45. 45. Summary
  46. 46. Functional considerations• Over 70 years ago Wilson introduced term ‘extra pyramidal’ motor system in his classic description of hepatolenticular degeneration : – Familial disorder of copper metabolism – Degeneration of striatum – Liver cirrhosis – Flapping tremor – Rigidity – K F ring on cornea• The corpus striatum and related nuclei exert their inflence on motor activities by the way of thalamic neurons that project upon and modulate the motor cortical areas
  47. 47. Functional considerations• The information from the frontal, prefrontal, and parietal areas of the cortex passes through the basal ganglia, then returns to the supplementary motor area via the thalamus.• The basal ganglia are thus thought to facilitate movement by channelling information from various regions of the cortex to the SMA.• The basal ganglia may also act as a filter, blocking the execution of movements that are unsuited to the situation.
  48. 48. • Dopamine neurons can be more meaningfully organized at a functional level into dorsal and ventral tiers.• The DORSAL TIER is formed by a medially–laterally oriented band of neurons that includes the dopamine-containing cells that are – (1) located in the medial ventral mesencephalon, – (2) scattered dorsal to the dense cell clusters in the substantia nigra, – (3) distributed lateral and caudal to the red nucleus.• Dorsal tier = low levels of dopamine = input from limbic-related structures = the pathophysiology of SCHIZOPHRENIA.• The VENTRAL TIER comprises 1. The dopamine neurons that are densely packed in the substantia nigra 2. The cell columns that penetrate into the substantia nigra pars reticulata.• Ventral-tier neurons = high levels of dopamine = projections to the sensorimotor regions of the striatum = the pathology of PARKINSONS DISEASE
  49. 49. Functional considerations• Clinically 2 types of disturbances are associated with diseases of corpus striatum :A. Dyskinesia : various types of abn. Involuntary movements 1. Tremor 2. Athetosis 3. Chorea 4. BallismB. Disturbances of muscle tone
  50. 50. Dyskinesia• Tremor : – Mc dyskinesia – Rhythical, alternating, abn involuntary motor activity having relatively regular frequency and amplitude – Paralysis agitans (Parkinsonism) reduce with voluntary movement – Cerebellar lesions : increase with voluntary movements – Paresis : with weakness – Emotional excitement : – Drug induced: – Disappears during sleep /GA : supporting the role of cortex in the neural mechanism of dyskinesias• Athetosis: – slow, writhing, vermicular involantary movements of esp. extremities – May involve axial muscles produce severe torsion
  51. 51. Dyskinesia• Chorea – Brisk , graceful series of sucessice involuntary movements of considerable complexity which resemble fragments of porpuseful voluntary movements – Distal portions of extremities (unlike ballismus), face, tounge and delutional musculature – Associated wit hypotonus – Sydenham’s chorea with RHD – complete recovery – Hunting ton’s disease – choreiform movements and progressive dementia• Ballism – A voilent , forceful, flinging movement, involves primarily prox.muscle – Represents most voilent form of dyskinesia – Almost always associated with discrete lesions in STN – Associated with marked hypotonus
  52. 52. DYSKINESIA - NEURAL MECHANISMS• Dyskinesia with excessive muscle tone = positive symptoms• Believed to be result of release phenomena= a lesion in one stucture removes the controlling and regulating influences which was previously exerted another neural mechanism.• This forms the basis of neurosurgical attempts to alleviate or abolish dyskinesia and rigidity without producing paresis. • Patients with paralysis agitans exhibit mask like face, infrequent eye blinking, slowness of movement, stooped posture, loss of associated movements = negative symptoms = due to destroyed neural structures
  53. 53. Basal ganglion lesions in Psychiatric Diseases
  54. 54. Basal ganglion lesions in Psychiatric Diseases• MDD : – One abnormality commonly observed in the depressive disorders is increased frequency of hyperintensities in subcortical regions such as periventricular regions, the basal ganglia, and the thalamus.• TICS : – Tics are defined as sudden rapid recurrent non-rhythmic stereotyped movements, gestures, or utterances, which may affect any part of the body, and typically mimic some aspects or fragments of normal behaviour. – Tourettes disorder = a diffuse process in the brain involving corticostriatothalamicortical (CSTC) pathways in the basal ganglia, striatum, and frontal lobes. – Several neurotransmitters and neuromodulators have been implicated, including dopamine, serotonin, and endogenous opioids. – Volumetric MRI studies = decreased volume of the basal ganglia – Typical neuroleptic medications block postsynaptic D2 (dopamine) receptors in the basal ganglia, decreasing dopaminergic input from the substantia nigra and ventral tegmentum and thus reducing tics.
  55. 55. Basal ganglion lesions in Psychiatric Diseases• ADHD : – Although the etiology of ADHD yet has to be determined, there is a growing consensus that the condition involves functional and anatomical dysfunction in the brains frontal cortex and basal ganglia segments of the cortico-basal ganglia-thalamo-cortical circuitry. – These areas support the regulation of attentional resources, the programming of complex motor behaviors, and the learning of responses to reinforcement.• OCD: – obsessive–compulsive symptoms could be associated with neurological disorders of motor control, including Tourettes disorder, Huntingtons disease, Parkinsons disease, as well as traumatic or infectious lesions of the basal ganglia – PET and functional MRI have generally demonstrated metabolic abnormalities in the circuits involving orbitofrontal/cingulate cortex and the basal ganglia—most particularly the caudate nuclei—in obsessive–compulsive patients. – Studies done at rest and during symptom provocation = selective increases in regional blood flow in the caudate and orbitofrontal cortex, which correlated with symptom intensity.
  56. 56. Reference• Kaplan and Saddock CTP 9th Ed• Malcom B Carpenter Neuroanatomy 3rd Ed• Atlas of the Human Brain and Spinal Cord (Jones & Bartlett, 2008)• OTP 2003Ed• Internet
  57. 57. Thank you