Neurodegeneration Flashcards
What structures are required for consolidation of declarative memory?
• Hippocampus and entorhinal cortex (medial temporal lobe structures) required for reinforcement (consolidation) of declarative memory
What projects to and from the entorhinal area?
o Projections to and from all over cortex are funnelled through hippocampus, entorhinal area.
o Entorhinal area has massive projection to cortex and receives massive projections from cortex
What are the earliest lesions which can be seen in Alzheimer’s disease?
Earliest lesions we see in Alzheimer’s is entorhinal cortex
What is the basis of declarative memory anatomically?
• Strengthened connections between cortical areas is the basis of declarative memory
What is important in recall of information anatomically?
• Activation of strengthened networks is the basis of recall
What is the function of the dorsolateral prefrontal cortex?
• Areas such as dorsolateral prefrontal cortex is important in network activation (recall) and storage
How is memory distributed in the brain?
• Memory distributed across modality-specific areas and association areas
o It’s really in the connections
Describe what ageing does to the brain
• Do not lose neurons as you age- may be minor loss of neurons
• Mild cortical atrophy
o Mainly white matter shrinkage
o Minor grey matter atrophy
• Get peroxidised lipids in neurons (lipofuscin)- but it is benign
• Most changes that do occur with age in the brain (permanent or temporary) relate to the cerebrovasculature
• Stroke (loss of blood flow) is the most common neurological disorder and a major cause of death
• Most subtle vascular changes may also occur- mild ischaemia, especially with atherosclerosis can cause temporary disability
Do most people get cognitive disorders or experience mild cognitive decline?
• Majority of people do not see cognitive disorders in their lifetime
o Most people will have some Alzheimer-type pathology but not sufficient to affect function
• Mild cognitive decline is common in late age
What are the problems with defining late age and what is the impact of this?
- Late age refers to more advanced years
- Definition of late age has changed in the last 50 years
- Need to be cautious when considering cross-sectional vs longitudinal design of population ageing studies
What is dementia?
• Dementia- a significant decline in at least 2 areas of higher cognition such as memory, language, planning, judgement, abstraction, calculation and personality- category term. A collection of clinical symptoms, not a disease.
What defines a syndrome within dementia?
• A constellation of symptoms define the syndrome
What are examples of specific dementia symptoms
• Specific dementia symptoms include- o Prefrontal areas affect judgement, impulsivity, emotional expression o Memory areas in MTL o Language areas o Modality specific areas o Higher association areas e.g. parietal o Behaviour: amygdala, hypothalamus, prefrontal areas o Striatum: habits, personality
Describe how dementia was referred to starting from 2013
• 2013- DSMV abandoned the term dementia in lieu of:
o Mild cognitive impairment (MCI)
Some cases of mild cognitive impairment may be prodromal dementia that is, person will go on to develop dementia
Major area of research clinically
o Severe cognitive impairment (dementia)
What are the trends of incidence vs prevalence of dementia and why?
• As a consequence of greater numbers of people living to later ages, the prevalence of dementia is increasing: however, the incidence is actually decreasing in many parts of the world
How many cases of dementia would occur in the next 30-35 years?
Estimated 1000000 cases in Australia in the next 30-35 years
What are different types of dementia?
• Types of dementia include: o Alzheimer’s disease o Vascular dementia o Frontotemporal dementias o Lewy body disease o HIV/AIDS related dementia o Korsakoff’s dementia
What percentage of all dementia cases does Alzheimer’s disease account for?
Alzheimer’s disease accounts for 50-70% of all dementia cases
What types of dementias are treatable?
• Some dementias may be treatable o Intracranial masses o Encephalitis o Meningitis o Vitamin deficiency o Depression-related dementia
Describe when Alzheimer’s disease is diagnosed
- Probable diagnosis during life based on cognitive features and progression
- Definitive diagnosis is post mortem, however the clinical assessment is now highly accurate
Describe the onset and progression of Alzheimer’s disease
- Insidious onset
* Slow (rather than abrupt or stepwise) progression
Describe the duration of Alzheimer’s disease
• Duration is 5-12 years, but likely long prodromal (disease has been there before the symptoms) period
o Mostly diagnosed retrospectively
Describe Alzheimer’s disease symptoms
• Memory signs appear early
o Repetition
o Getting lost
o Inability to do calculations and following conservations
o Trouble orienting to space and time
o Losing things
o Hiding things
• Early on, daily activities of living are intact but may need instruction, breaking down tasks
• Other cognitive signs appear later
o Behavioural changes (agitation, paranoia)
o Aphasias
o Apraxias
o Activities of daily living (dressing, eating, bathing)
o Agitation
What is exclusion criteria for Alzheimer’s disease diagnosis
• Exclusion criteria for alzheimer’s disease diagnosis
o Movement disorders
o Abrupt onset
o Delirium, seizures, focal signs
What are the risk factors for Alzheimer’s disease?
• Risk factors for Alzheimer’s disease o Age- highest risk factors o Genetics- less than 1% of cases have a defined genetic link Autosomal dominant mutations- Amyloid Precursor Protein (APP), Presenilin 1, Presenilin 2 o Cardiovascular risk factors Diabetes type II Midlife hypertension Smoking Atrial fibrillation Previous stroke High cholesterol o Head injury o Low educational attainment (may be study bias or socioeconomic factors)
What 2 markers does post mortem diagnosis of Alzheimer disease require?
Extracellular amyloid deposits
Intracellular neurofibrillary tangles
Describe the production and deposition process and location of extracellular amyloid deposits, as well as their correlation with Alzheimer’s symptoms in Alzheimer’s disease
Extracellular amyloid deposits
• Amyloid is produced by abnormal cleavage of the amyloid precursor protein
• Some familial forms of the disease associated with APP mutations
• Amyloid beta is deposited extra-neuronally in plaques in the brain but in particular in cortical layers
o Not inside of cells, but outside of cells
• Amyloid beta is deposited within and around blood vessels
• Not well-correlated with dementia symptoms compared to tangles
Describe the production and deposition location of intracellular neurofibrillary tangles in Alzheimer’s disease
Intracellular neurofibrillary tangles
• Occurs through
o Microtubule associated protein tau becomes hyper-phosphorylated
o Hyperphosphorylated tau (Hp-tau) fills the neuron
o Hp-tau forms fibrils that collect into tangles within neurons
o Neurons eventually die, tangle left behind (ghost tangle)
• Inside neurons
• There is high density of tangles in hippocampus and entorhinal cortex
Describe the stages of AD symptomatically and neurofibrillarily
• Stages of AD-
o Stages I-III
No symptoms
Neurofibrillary tangles start to appear in hippocampus and entorhinal cortex
o Stages III-IV
Subtle symptoms appear- memory affected early
Will have lots of neurofibrillary tangles in medial temporal lobe
o Stages V-VI
Other cognitive symptoms- clinical diagnosis
Tangles have spread to rest of cortex- temporal neocortex, then limbic and association cortex
• Tangles are also found in hypothalamus, amygdala and brainstem
What does progression of Alzheimer’s disease cognitive dysfunction correlate with? Explain.
• Progression of alzheimer’s disease cognitive dysfunction correlates with the location of neuronal pathology
o Alzheimer’s disease- early
Anterograde amnesia- no new memories
Atrophy and neuronal pathology (tangles) in hippocampus/entorhinal cortex
o Alzheimer’s disease- later
Retrograde- old memories lost
Previously consolidated memories erode
Atrophy and neuronal pathology (tangles) in the neocortex
• Disconnection of the memory trace as nodes- neurons- in the network succumb to tangle formation
What is frontotemporal dementia and what area of the brain does it affect?
• FTD is a group of disorders/syndromes with different aetiologies, frequencies, progression, symptoms and genetics
• They have in common atrophy in frontal and temporal lobes: striking specificity
o But different proportions of frontal and temporal atrophy- frontal atrophy is usually the most profound
o Symptoms more likely to be frontal related symptoms
What percentages of dementias does frontotemporal dementia account for?
• FTD accounts for just about 10-15% of dementias overall, all ages considered
o Frontotemporal dementia is relatively rare compared to AD
For people under 50 years, what percentage of dementia cases does FTD account for? What is the onset of FTD?
• For persons under 50 years, FTD accounts for more than 50% of dementias
o Large proportion of patients have young onset (40s and 50s but may be as young as 20 years)
Compared to Alzheimer’s disease, what proportion of patients have a genetic link to frontotemporal dementia
• Larger proportion of patients have genetical link compared to AD
What are the symptoms of frontotemporal dementia?
• Clinical features of FTD related to brain regions
o Behavioural abnormalities related to prefrontal areas
Decreased initiative
Social disinhibition, impulsivity, loss of restraint
Poor planning
Emotional blunting, difficulty regulating emotion
Stereotypical behaviours
• Repetitive behaviours, mimicking behaviours, compulsive behaviours
o Aphasias
Some forms of FTD have primarily a language dysfunction
Related to atrophy in Wernicke’s and Broca’s language areas
o Memory dysfunction- temporal lobe areas and DLPF cortex
Usually appears later, can be a minor feature and often not as severe as in AD
o Movement disorders
Some subtypes of FTD show parkinsonism
• More likely to have an early age of onset (midlife- 40-50 years)
What is the duration of symptoms for frontotemporal dementia
o 2 to 15 year duration of symptoms
What is the problem with understanding frontotemporal dementia? What is currently known about the process of frontotemporal dementia?
• Problems with understanding FTD
o Microscopic pathology in FTD not well understood compared to AD
o Frontotemporal dementia was once called Pick’s disease (protein also made of tau)
o However, most cases of FTD do not have Pick bodies (only 5% had Pick bodies), so most cases no longer classified as Pick’s disease
o Inflammation is common: astrocyte and microglia reaction
What are the causes of Parkinson’s disease?
• Causes-
o Genetics (15%)
Associated with dysfunction of pre-synaptic proteins or mitochondrial dysfunction
More likely with early onset forms of disease (40-45)
o Prions (infectious agents: alpha synuclein, gut)
Parkinson’s disease could spread from the gut from the vagus nerve and up to brain- transmits alpha synuclein to the brain
o Head trauma (vibrations)
o Toxins (MPTP)
Straight to dopaminergic cells in substantia nigra pars compacta and kills them
How can you protect from Parkinson’s neurodegeneration and how does each method work?
• Protectors from neurodegeneration
o Anti-oxidants-> have been shown to help a neuron in distress and help them survive
o Exercise-> releases growth hormones in brain to help cells in distress survive better
o Coffee-> stimulates locomotion
o Smoking -> stops breakdown of dopamine at synapse
What are the motor signs of parkinson’s disease
o Motor signs- diagnosis with 2 of these signs- one has to be tremor or bradykinesia Resting tremor (4-7 Hz) • Starts unilateral but becomes bilateral Lead-pipe rigidity (hypertonia) • Muscles become stiff Akinesia • No movement- almost frozen Bradykinesia • Slow movement Loss of posture reflex Hypomimia • Expressionless face Dysphagia • Trouble swallowing Dysarthria • Problems with speech Micrographia • Very small writing Cog-wheel rigidity • No smooth hand movement Festinant gait • Short, sharp steps Freezing
What are the non-motor symptoms of Parkinson’s disease
o Non-motor symptoms (often occur prodromally) Anosmia (smell) Sleep Fatigue/Apathy Psychiatric/depression issues Somatosensory/ pins and needles Gastrointestinal Autonomic Cognition (towards the end of the disease course)
What are the two forms of Parkinson’s disease
• Two forms of the disease
o Tremor dominant form of disease- tremor but not necessarily akinesia, bradykinesia or rigidity
Better form of the disease
o Akinetic form of disease- but don’t necessarily have tremor
Worst form of the disease
What neurons are lost in parkinson’s disease? How much of these neurons need to be lost before the disease becomes apparent?
• Drop of substantia nigra pars compacta dopaminergic cells and loss of their terminations in the striatum (dopaminergic terminals)
o 50-70% loss needed before signs of the disease become evident
• Some serotoninergic and noradrenergic loss
How does Parkinson’s disease progress?
• Progressive
o Continued toxin/gene/prion (self-propagation)
o Glial attack neurons and cause them to become dysfunctional and die
What are pathological features of Parkinson’s disease
• Lewy body (alpha synuclein)
• Mitochondria dysfunction caused by alpha synuclein
o Lowered ATP production
o Increase in reactive oxygen species which will disrupt neurons and cause it to die
What is the mechanism of Parkinson’s disease
• Mechanisms
o Due to destruction of dopaminergic direct pathway (nigrostriatal pathway), Indirect pathway become overactive which inhibits GABAergic cells in globus pallidus external, which project to subthalamic nucleus
o Subthalamic nucleus becomes overactive- its glutamatergic cells (excitatory) project to globus pallidus internal which stimulates it
o Globus pallidus internal has inhibitory projections to the thalamus
Too much inhibition to thalamus which means it can no longer project to the cortex-> suppression in cortex-> movement is suppressed -> causes motor symptoms (tremor, akinesia, bradykinesia, rigidity)
What are current treatments of Parkinson’s disease?
• Drugs: dopamine replacement theory
o 1st line treatment
• Surgery: disrupt abnormal circuit
o 2nd line (combination with drugs)
What is the problem with drug therapy for Parkinson’s disease and how may this problem occur?
o Less effective 5-8 years: on-off effect
Sometimes drugs work fine, sometimes they work too much, or sometimes it doesn’t work enough
o May be because of:
Change in δ receptors
Dysfunctional uptake mechanisms
Progressive cell death -> less cells to stimulate and hence less effective
How does surgery for Parkinson’s disease work?
• Surgery: disrupt abnormal circuit
o 2nd line (combination with drugs)
Drug dose reduces from 30-50%
o Subthalamic target to inhibit the subthalamic target
o Lesion/deep brain stimulation (DBS of about 100Hz)
Lesion- burn or freeze subthalamic nucleus
DBS- electrode above subthalamus with powerpack in clavicle that drives the electrode
• At high frequency, it inhibits subthalamic nucleus
What is the problem of current treatments for Parkinson’s disease
• Treatment problems- drugs and surgery largely symptomatic
What are potential future treatments for Parkinson’s disease?
o Need to slow or stop pathology Stop the prion (alpha synuclein) Stimulate mitochondria Transplants: foetal substantia nigra pars compacta inserted into basal ganglia-> foetal cells will grow and make connections with right cells in substantia nigra Stems: new cells Gene therapy: δ phenotype
What is the problem with transplanting foetal substantia nigra cells in an adult brain to treat Parkinson’s disease?
- Foetal cells have no signals in adult brain, so they do not know where to go
- Can’t control dopaminergic output
How does gene therapy δ treatment for Parkinson’s disease work?
- Inject viral vector in subthalamic nucleus, it changes phenotype of subthalamic nucleus and turns its cells into GABAergic cells
- Seems to be effective
What is chorea and what are its causes/types?
• Involuntary dance
• Causes/types
o Huntington’s chorea- midlife diagnosis (40 years old) and often fatal
Genetic mutations in group of cells in caudate putamen
o Sydenham’s chorea- develops in children: temporary and associated with rheumatic heart’s disease
What are signs of chorea?
• Signs
o Jerks and figits (distal)
Dyskinesia
What is the pathology of chorea?
• Pathology
o Decreased GABA-Enkephalin cells (in indirect pathway) of caudate putamen
Lowered caudate putamen volume
Lowered indirect pathway
What are the mechanisms of chorea?
• Mechanisms
o Nothing to switch off GABAergic neurons in globus pallidus externis, which closes down the subthalamic nucleus
o Means that subthalamic nucleus can’t stimulus globus pallidus internis to inhibit the thalamus
o Overactive thalamus which means too much activity in cortex which makes too much movement
What is ballismus and what it can result in?
o A subthalamic nucleus lesion caused by an infarct from posterior cerebral artery
Posterior cerebral artery supplies subthalamic nucleus
If there is problem with this artery, then lose the subthalamic nucleus (death of tissue)
o This produces violent dyskinesia
What is the function of the thalamus?
Sensory relay, motor modulation, limbic and associative functions, influences cortical activities and sleep
What is the function of the hypothalamus
• Involved in autonomic, endocrine and other homeostatic functions
o Regulation of circadiane rhythms
o Needs and behavioural drives
o Limbic system circuits
What is the function of the subthalamus?
• Motor modulation, especially through the globus pallidus
What is the function of the epithalamus
- Involved in onset of puberty and biological rhythms
* Secretes melatonin
What are the nuclei of the thalamus?
• Ventral posterior nucleus • Motor thalamus o Ventral lateral nucleus and ventroanterior nucleus • Pulvinar nucleus • Medial geniculate nucleus • Lateral geniculate nucleus • Limbic thalamus o Anterior nucleus (tubercle) o Mediodorsal nucleus
What is the function, input and output of the ventral posterior nucleus?
• Ventral posterior nucleus-somatic sensory system and projects to cortex of postcentral gyrus, but receives dorsal column, trigeminal and spinothalamic input
What is the function, input and output of the motor thalamus?
o Ventral lateral nucleus and ventroanterior nucleus -parts of the motor system which projects the motor cortex of the precentral gyrus. Motor relay between basal ganglia and cortex, NO output to lower motor neurons
- –Regulates execution of motor plans through influence on cortical motor output and by feedback into basal ganglia and cerebellar circuits
- –Thalamus projects onto motor cortex to readjust and increase accuracy of movement
- –The basal ganglia receive input from the cortex, project out to the thalamus which then projects to areas of the cortex involved in motor planning
What is the function, input and output of the pulvinar nucleus?
• Pulvinar nucleus-connected to the association cortex and plays a role in guiding attention. Visual input directly from retina and indirectly via superior colliculus. Visual tracking integration with body position
Adjusts head position towards objects in visual field
–Can receive auditory input from inferior colliculus (auditory) and vestibular centres, but is highly visually-oriented
What is the function of the medial geniculate nucleus?
• Medial geniculate nucleus-relays information to auditory cortex from the inferior colliculus
What is the function of the lateral geniculate nucleus?
• Lateral geniculate nucleus-relays information to visual cortex
What is the input and output of the limbic thalamus? What is the purpose of these
• Limbic thalamus
o Anterior nucleus (tubercle) -input from mammillary bodies, output to cingulate cortex
—-Attention, mood and pain
o Mediodorsal nucleus- input amygdala and entorhinal cortex, output to prefrontal areas including dorsolateral prefrontal cortex
—–Working memory, effortful processing, decision making, moderating social behaviour
Does the hypothalamus recieve input from the amygdala?
Yes
How does the hypothalamus exert its endocrine functions?
• Hypothalamus exerts its endocrine function by releasing hormones into the blood stream via the hypophyseal portal system.
o Behaviours related to these functions are coordinated through centres such as the amygdala and peri-aqueductal grey areas
Describe the composition of the epithalamus and its inputs
- Includes pineal gland and habenula
* Receives light information from the retina indirectly via the suprachiasmatic nucleus of the hypothalamus
Where exactly is the subthalamus located?
o Subthalamus is above the substantia nigra and slightly lateral and anterior to the red nucleus of the midbrain
Why is the internal capsule important?
The internal capsule contains the major pathways that allow information to be transferred between the cerebral cortex and the spinal cord, brainstem and subcortical structures such as the thalamus and basal ganglia
Describe the thalamus as a sensory gateway system
- Performs fine-tuning and adjusting of information
- Thalamic processing can set the level of input to the cortex, increasing or decreasing the volume of olfaction
Describe the thalamus as a motor relay system
Thalamus receives input from the basal ganglia and cerebellum and relays the information to the motor and premotor (motor association, supplementary motor) areas
-This is a modulation pathway of motor systems that support ongoing movement
Does the thalamus project directly to lower motor neurons?
NO
Describe the thalamus as an arousal system
Thalamus has a pivotal role in influencing different arousal states
- Thalamus imposes a rhythm on cortical activity
- This rhythm is inhibited during waking and released during sleep
- As rhythmic thalamic output to the cortex increases, sensory input to the cortex decreases
- In sleep, sensory input to the cortex is inhibited
Describe the role of the thalamus in attention and complex reflexes
- Thalamus helps focus attention on key information
- -Pulvinar: eye tracking, posture and vision
- -Mediodorsal nucleus: cognitive attention
Describe the role of the thalamus in limbic functions-emotion and memory
Thalamus modulates emotional and motivational response and memory, by the mediodorsal and anterior thalamic nuclei
What are the parts of the hippocampus?
- Dentate gyrus
- Hippocampus proper
- Subiculum
Do the cerebellum and basal ganglia have direct access to the spinal or brainstem lower motor neuron pools?
NO
What is the role of basal ganglia
o Basal ganglia has a role in planning, executing and learning motor functions, procedural learning and other cognitive functions such as habits, motivation and reward
What do lesions of the subthalamic nucleus produce?
o Subthalamic nucleus- contralateral hemiballismus (dramatic uncontrolled flinging motions of the body)
What do lesions of the substantia nigra produce?
o Substantia nigra- parkinsonism (includes resting tremor, stooped posture, slow movement and difficulty initiating movement)
What do lesions of the striatum produce?
o Striatum- huntington’s disease (chorea)- restless jerkless movement, as well as personality changes and procedural memory deficits
What are the components of the basal ganglia?
Basal ganglia • Caudate nucleus • Putamen • Globus pallidus o Globus Pallidus internal o Globus pallidus external • Nucleus accumbens • Substantia nigra o Pars compacta (SNc) o Pars reticulata (SNr) • Subthalamic nucleus
Where is the caudate nucleus found?
• Caudate nucleus
o Follows the contours of the lateral ventricle
How is the putamen separated from the globus pallidus?
o Putamen separated from globus pallidus by white matter capsule
Where is the nucleus accumbens and what is its function? Where does it output?
• Nucleus accumbens
o Area at the inferior merger of head of caudate and putamen
o Reward and reinforcement
o Outputs to the globus pallidus
Where is the globus pallidus and what inputs into it and where does it output?
o Lateral border of the internal capsule
o Major output of the basal ganglia, projecting to the thalamus, which then projects to the cortex
What is the ansa lenticularis?
Fibres that stream medially across the internal capsule, from the globus pallidus to the thalamus
Where is the substantia nigra pars compacta and what does it contain?
o Pars compacta (SNc)
Dorsal black zone- cells are rich in dopamine and melanin
Where is the substantia nigra pars reticulata and what does it contain?
o Pars reticulata (SNr)
Surrounds the SNc rim, adjacent to cerebral peduncle, cells lack pigment
Rich in iron and contain no dopamine
Where is the subthalamic nucleus and what is contained in it?
o Subthalamic nucleus is related to medial border of the internal capsule and lies ventral to the thalamus
o Contains many glutamatergic neurons and has rich connections with the globus palllidus
What are the functions of the cerebellum?
o Cerebellum Maintains muscle tone and posture Coordinates eye and body movement Maintains equilibrium Smooth movements Plans precise movements Coordinates and retains motor skills memory
What are the 3 sections of the cerebellum?
- Cerebrocerebellum (lateral anterior and posterior lobes separated by primary fissure)
- Spinocerebellum (vermis)
- Flocculonodular lobe (vestibulocerebellum)
What is the function of the cerebrocerebellum?
o Regulates planning of complex, skilled and intentional movement
What are the major inputs and outputs of the cerebrocerebellum
o Receives input from the cerebral cortex (especially motor and somatosensory cortex) which comes from the pontine nuclei via the middle cerebellar peduncles
o Major output is to the motor thalamus and to the red nucleus to control movement through the brainstem and spinal cord
What do lesions of the cerebrocerebellum result in?
o Lesions- incoordination of skilled movement
What is the function of the spinocerebellum in the cerebellum?
o Controls stereotyped movement and posture
What are the inputs and outputs of the spinocerebellum?
o Via cortical and brainstem projections to the spinal cord by processing the timing and duration of contractions in antagonistic muscle groups in conjunction with control of trunk muscles and posture, allowing target movement to be reached with precision
o Receives input about proprioception from the dorsal columns of the spinal cord and from trigeminal nerve
What are the results of lesions of the spinocerebellum?
o Lesions- cause disturbances in coordination, problems with rapid movement, ataxia, staggering and broad based gait
What is the function of the flocculonodular lobe?
o Coordinates balance, posture and eye movement in accordance to vestibular input
What are the inputs and outputs of the flocculonodular lobe?
o Receives vestibular input and sends information back to the medial and lateral vestibular nuclei
o Receives visual input from the superior colliculi and from visual cortex
What are the results of the flocculonodular lobe?
o Lesions- cause disturbances in balance and in eye movement
What is asynergia?
• Asynergia- loss of coordination of motor movement
What is dysmetria?
• Dysmetria- inability to judge distance and when to stop moving
What is disdiadochokinesia?
• Disdiadochokinesia- inability to perform rapid alternating movement
What is intention tremor?
• Intention tremor- movement tremors
What is ataxic gait?
• Ataxic gait- staggering, wide based walking
What is hypotonia?
• Hypotonia- weak muscles
What is ataxic dysarthria?
• Ataxic dysarthria- slurred speech
What is nystagmus?
• Nystagmus- abnormal eye tracking movements
What is the lentiform nucleus?
Putamen- lateral 2/3
Globus pallidus- medial 1/3
What is the striatum?
Caudate and putamen
