Neurology Flashcards
What is Multiple Sclerosis?
- MS is an autoimmune, inflammatory, demyelinating & degenerative condition of the central nervous system.
- The immune trigger is unknown but the targets are myelinated Central Nervous System (CNS) Tracts.
- In regions of inflammation, breakdown of the blood–brain barrier occurs and destruction of myelin ensues, with axonal damage, gliosis and the formation of sclerotic plaques.
- Plaques (MS lesions) may form in the CNS white matter in any location (and also in grey matter); thus, clinical presentations may be diverse.
What is the physiological theory behind MS?
- It’s a B cell and T cell disorder
- activated T cells enter the CNS → release chemicals that cause inflammation and de-myelination
- T-cells also activate B cells → these B cells go on to produce antibodies and stimulate the other proteins that cause further damage to the CNS
- there is initial damage to that region which presents as clinical i.e optic nerve neuritis but is also proceeded by re-myelination which presents as clinical recovery
- however, there can be some deficit, especially with subsequent attacks → more neuronal damage and brain atrophy which can be seen in MRI scans
What is the epidemiology of Multiple Sclerosis?
- It’s the leading cause of the nontraumatic disabling neurological conditions in you adults
- Starts between 20-40 y/o
- 5% of cases occur in childhood (rare in under 10y/o)
- ~2.5 million people are affected worldwide
- 100,000 people in the UK have MS (~1/600)
- the lifetime risk in the general population is ~1:30
- Women are twice as likely to develop MS as men
- MS incidence is higher in colder climates Vit D deficiency?
What are the Genetic factors in the occurrence of Multiple Sclerosis?
- Most common in the white population
- Northern European descent
- HLA DRB1*1501 on chromosome 6p21
- Non-HLA genes also identified (IL7RA &IL2RA)
- Familial recurrence rate of about 20%
- Siblings 5%; parents 2% & children 2%
- Reduction in risk changes from 3% in first degree relatives to 1% in 2nd & 3rd relatives
- However, alteration in the risk of MS depending on the age of migration
suggests it’s not only genetic factors but also environmental
What is the link between Viral infection and Multiple Sclerosis?
- 40% of new clinical symptoms are associated with a viral infection
- 10% of infections in MS patients are followed by a relapse
- Relative risk of contracting MS increases with age of infection with measles, mumps, rubella and EBV (up to age 12-15 years old)
- EBV infection as young adult – 8x risk of MS
What is a Clinically Isolated Syndrome?
- A clinically isolated syndrome (CIS) is an acute or subacute neurological syndrome
- A CIS is usually the first clinical event in an MS patient
- MS will develop in 80% of patients with a CIS, however, a CIS is not entirely predictive of MS hence other differentials need to be considered as a CIS covers a broad spectrum of syndromes
- MS is not the only recurrent demyelinating disease i.e adrenoleukodystrophy
Which CIS symptoms are characteristic of MS?
- Painful optic neuritis
- Partial acute transverse myelitis
- Lhermitte’s symptom
- Bilateral internuclear ophthalmoparesis (INO)
- Paroxysmal dysarthria\ataxia
- Tonic seizures
What is Lhermitte’s syndrome?
when does it occur?
An electric shock like sensation that affects the spine and neck. It is often sporadic, does not last long and may recur
- this is seen in MS, cervical spondylosis, cervical tumour and b12 deficiency
Explain dissemination in time and space in relation to Multiple sclerosis
Dissemination in space: looking for one or more lesions in the following regions the periventricular, cortical, Infratenorial, spinal cord
Dissemination in time: a new T2 and/or gadolinium-enhancing lesion(s) on follow-up MRI, with reference to a baseline scan, irrespective of the timing of the baseline MRI. The simultaneous presence of symptomatic gadolinium-enhancing and non-enhancing lesions at any time (shows newer and older lesions, occurring within 6>8 weeks)
What is Uhtoff’s phenomenon?
When symptoms of MS are brought on by a period of increased body temperature
i.e visual disturbances after taking a hot shower, sauna, or having a fever
What is the typical and atypical presentation of optic neuritis in MS?
What is the typical and atypical presentation of Isolated Brain Stem Syndrome
What is the typical and Atypical presentation of Isolated Spinal Cord Syndrome?
What are the differentials for individuals presenting atypically with Optic Neuritis
Atypical presentation → no pain, retinal exudates, retinal haemorrhages severe disc swelling, no visual recovery
- Ischaemic Optic Neuritis (ON)
- hereditary ON
- Infiltrative ON
- Inflammatory (sarcoid, lupus)
- infection (syphilis, Lyme, viral)
- Toxic/Nutritional
- Retinal disorders
What are the differentials for individuals presenting atypically with isolated Brain Stem Syndrome
Atypical presentation → hyperacute onset, vascular territory signs e.g lateral medullary syndrome (sensory deficits), age >50, trigeminal neuralgia, fluctuating ocular/bulbar weakness, non-remitting, fever, meningism
- Ischaemic haemorrhagic (cavernous angioma)
- Infiltrative
- Inflammatory (sarcoid, lupus)
- Infection (syphilis, listeria, Lyme, viral)
- Toxic
- Nutritional
- Central pontine myelinolysis
- Neuromuscular
What are the differentials for individuals presenting atypically with Isolated Spinal Cord Syndrome
Atypical presentation → hyperacute onset or insidiously progressive, complete transverse myelitis, sharp sensory level, radicular pain, areflexia, failure to remit
- Compression e.g intervertebral disc, tumuor
- Ischemia/ infarction
- Other inflammatory disease e.g neuromyelitis optica, sarcoid, lupus, Sjorgens
- Infection e.g syphilis, lym, viral, TB
- Toxic/nutritional/metabolic e.g B12 deficiency, NO toxicity, copper deficiency
- Arteriovenous malformation
- non-cord mimics e.g Guillain-Barré syndrome, myasthenia gravis
What is the EDSS and what is it used for?
Expanded Disability Status Scale
- when an EDSS of 3 is reached the disease becomes irreversible
- the earlier txt starts the better the chances of delaying progression of the disease to this state
What is the long term implication of MS attack relapses?
the lower the number of relapses within the first 2 years of diagnosis the longer the time they have an EDSS less than 6 therefore the better their mobility
The interval between the attacks can also be predictive of disability from the disease onset
Patients with a short interval (0–2 years) reached DSS 6 and DSS 8 quicker than those with a long interval (e.g. 3–5 years or 6+ years)
How can the baseline Brain MRI lesions be used to diagnose MS or predict prognosis?
- the presence of a single lesion on a baseline MRI scan increases the risk of conversion to CDMS by around 80% versus 20% on those with a normal MRI
- If you have one or more lesions it didn’t really change this risk very much
- Those with more lesions tended to have a greater disability. But this trend showed great variability
- The location of the lesion can be an indicator of a long-term disability: ptx with at least 2 infratentorial lesions had a worse outcome at follow-up
- Lesion volume continues to increase for at least 20-years in relapse onset MS patients and the rate of lesion growth is 3 times higher in those who developed Secondary Progressive MS than those who remain Relapsing-Remitting MS
What can we learn from the appearance of grey and white matter on MRI scans about the prognosis of multiple sclerosis
GM, but not WM, fractions correlated with disability & lesion load
GM atrophy rate (expressed as a fold increase from the control subjects) increased with the disease stage
What is epilepsy?
- a recurring unprovoked (spontaneous) seizures
- acute symptomatic seizures are provoked by acute insults such as
- stroke, infection, alcohol withdrawal, or a metabolic disturbance
What types of seizures are there?
- Primary generalized onset: electrical discharges appear to start over the whole brain at the same time on EEG
- Partial/focal onset: electrical discharge appears to start in one cortical region and then may remain localized or may spread over the whole brain - secondary generalized
![](https://s3.amazonaws.com/brainscape-prod/system/cm/389/120/022/a_image_thumb.png?1604341452)
What are the classifications of Idiopathic (Primary) Generalized seizures?
- Limited repertoire of seizures
- Tonic-clonic seizures (“grand mal”)
- Absences (“petit mal”)
- Tonic seizures
- Atonic seizures
- Myoclonic seizures
Give an overview of what Idiopathic Generalized Seizures are?
- Onset in childhood or adolescence
- Usually no focal symptoms/signs
- Often a number of seizure types cluster
- A polygenic cause is presumed with no identifiable structural lesion on imaging
- Generalized (all leads) spike and wave discharges on EEG may be induced by hyperventilation, and on photosensitivity testing
- Provoked by sleep deprivation
What is Juvenile Myoclonic Epilepsy (JME? - give an overview
- Commonest form of primary generalized epilepsy 3-12% all epilepsy
- Juvenile onset, probably lifelong
- Early morning myoclonic jerks (ask)
- Photosensitive, sleep deprivation triggers
- +/- absences
- generalized tonic-clonic seizures – occur without warning
Give an overview of the presentation of Generalised Tonic-Clonic Seizures “grand mal”
- sudden onset without warning in primary generalised epilepsy
- Tonic phase
- continuous muscle spasm, fall, cyanosis, tongue biting, incontinence
- Clonic phase
- rhythmic jerking slows and gets larger in amplitude as the attack progresses
- Ends; the duration is typically 1-3 minutes
- Post-ictal (post-seizure) phase
- coma, drowsiness, confusion, headache
- muscle aching
- red/blue, wakes in ambulance/A&E
Give an overview of Absences “petit mal”
- Abrupt, short, 5-20 seconds
- Multiple times/day, can lead to learning difficulties
- Unresponsive, amnesia for the gap, rapid recovery
- Tone preserved (or mildly reduced)
- If absences only, tend to remit in adulthood (childhood absence epilepsy)
What ways are there Focal Onset Seizure?
- a simple partial seizure where the patient is aware (used to be an aura)
- focal seizure with awareness
- a complex partial seizure- aura/warning with a level of reduced awareness
- focal seizure with reduced awareness
Where d partial seizures frequently present themselves in the lobe?
- Temporal lobe - 70%
- Frontal lobe - 25%
- Occipital lobe - 4%
- Parietal lobe - 1%
Give temporal lobe seizures by aetiology
- Hippocampal sclerosis: 50%
- have a history of febrile convulsion
- Tumour: 18%
- Birth Hypoxia: 10%
- Vascular: 10%
- Post Traumatic: 8%
- Other: 4%
What are the symptoms and signs of temporal lobe epilepsy?
- hallucinations of taste, speech and /or smell, visual distortion; memory déjà vu and jamais vu
- epigastric rising sensation (over humpback bridge)
- fear, elation, low mood
- pallor/ flushing/ heart rate changes (can mimic panic/hyperventilation attacks)
- automatisms- semi-purposeful limb movements
- Oral automatisms- lip-smacking, chewing movements
- dystonic posturing (limb rises)
- speech disturbance (dominant hemisphere onset) last 1-3 minutes typically
![](https://s3.amazonaws.com/brainscape-prod/system/cm/389/120/032/a_image_thumb.png?1604347874)
What are the symptoms of a frontal lobe seizure?
- brief 10-30 seconds, rapid recovery, frequent
- predominantly nocturnal
- forced head /eye deviation to the contralateral side
- motor activity often bizarre, thrashing
- often misdiagnosed as non-epileptic
- ictal EEG (during the seizure) is often normal
- Jacksonian spread with Todd’s paresis
- automatisms, dystonic posturing for example
- a fencing posture (overlap TLE)
![](https://s3.amazonaws.com/brainscape-prod/system/cm/389/120/033/a_image_thumb.png?1604348339)
What are Parietal lobe epilepsy symptoms?
- positive sensory symptoms (unlike TIA/stroke)
- tingling, pain
- distortion of body shape/image
- Jacksonian march of positive sensory symptoms
What are Occipital lobe epilepsy symptoms?
- typically simple visual hallucinations -balls of coloured or flashing lights
- amaurosis (blackout or whiteout) at onset -25%
What anti-epileptic drugs make myoclonic jerks and absences worse?
- Phenytoin
- treats tonic-clonic seizures
- safe to use in status epilepticus (when a seizure lasts more than 5 minutes or are close together)
- Carbamazepine,
- Gabapentin,
- Pregabalin
Which type of seizure patient would you give a scan to?
- Jacksonian motor or sensory seizures
- Patients with focal neurological deficit (including a temporary unilateral Todds paresis)
- Alcohol withdrawal seizure; only scan if subdural haematoma suspected fall, hit head, found on the floor, bruising on head
What is the physiological representation of Epilepsy?
- Epilepsy represents a hyperexcitation or a failure of inhibitory regulation, either focally (e.g. motor cortex, temporal cortex) or generally (whole cortex at once)
How are epileptic episodes physiological caused?
- Na+ channel inactivation too slow in excitatory neurons
- Reduced number of functional Na+ channels in inhibitory neurons
- Reduced number of functional K+ channels in excitatory neurons
- Mutated ion channels: voltage-gated and ligand-gated ion channels
How do Na+ channel dysfunctions lead to epilepsy?
Na+ channel inactivation too slow in excitatory neurons
- e.g., generalized epilepsy with febrile seizures plus (GEFS+)
- a point mutation in part of Na+ channel (β subunit) –> abnormally slow inactivation
- action potential repolarization impaired
Reduced number of functional Na+ channels in inhibitory neurons
- e.g., generalized epilepsy with febrile seizures plus (GEFS+)
- missense mutations or truncated protein results in reduction or loss of Na+ channel function
- action potential generation impaired
How do K+ channelopathies lead to epilepsy?
Reduced number of functional K+ channels in excitatory neurons
- e.g., benign familial neonatal convulsions
- defect in KCNQ2 or KCNQ3 K+ channel subunit –> impaired activation
- action potential repolarization impaired
Explain the development of Focal (partial) seizures
- synchronized ‘paroxysmal depolarizing shift’ (PDS, 20 to 40 mV, lasting 50 to 200 ms) overcomes inhibition
- increased extracellular K+ due to neuronal damage or reduced uptake by the astrocytes as well as glutamate release from neurons or astrocytes contribute to PDS
- during the PDS trains of action, potentials occur
- hippocampal neurons have similar responses under normal conditions, making the hippocampus more prone to seizures than the neocortex
- Focal seizures may spread to other brain regions along the normal neuronal pathways and may also show secondary generalization if the activity spreads to the thalamus (tonic clonic seizure)
![](https://s3.amazonaws.com/brainscape-prod/system/cm/389/120/042/a_image_thumb.png?1604351267)
Explain the development of Primary Generalized seizures.
- Primary generalized seizures reach the cerebral cortex via normal neuronal pathways from the thalamus
- e.g. tonic clonic seizure; absence; juvenile myoclonic epilepsy
- pathways originate in the brainstem and are normally involved in regulating the sleep/wake cycle and arousal of the cerebral cortex
- Ca2+ channels and inhibitory GABA receptors in thalamic neurons have been implicated in ‘spike and wave’ seizures, showing that inhibition (the wave) is preserved
![](https://s3.amazonaws.com/brainscape-prod/system/cm/389/120/043/a_image_thumb.png?1604351243)
What is the general action of Anti-epileptic drugs?
- work to inhibit Glutamate
- this is an excitatory molecule in the brain
- work to increase GABA activity
- this is an inhibitory molecule in the brain
What AEDs work by inhibiting the excitatory process in neurons?
- Phenytoin, Carbama/ Oxcarba-zepine, Eslicarbazepine acetate, Lamotrigine, Lacos/ Zonis-amide
- inhibits voltage-gated Na+ ion channel
- Ethosuximide
- inhibits Ca2++ entry into postsynaptic neuron
- Retigabine
- increases excite of K+ from the postsynaptic neuron
- Perampanel
- inhibits the AMPA receptor which glutamate binds to and allows NA+ into the postsynaptic neuron
![](https://s3.amazonaws.com/brainscape-prod/system/cm/389/120/045/a_image_thumb.jpg?1604353988)
What AEDs work by increasing the activity of the inhibitory process in neurons?
- Levetiracetam
- increases activity of SV2A- regulates action potential-dependent neurotransmitter release
- Retigabine
- increases the activity of KCNQ K+ channels in the pre and postsynaptic neuron
- Gabapentin, Pregabalin
- inhibit alpha-2-beta-subunit of Ca2+ channels in the presynaptic neuron
- Tiagabine
- Inhibits GAT-1 in presynaptic neurons and on glial cells
- Benzodiazepines, Barbiturates
- increases activity of GABAA more Cl- moved into the postsynaptic neuron
![](https://s3.amazonaws.com/brainscape-prod/system/cm/389/120/046/a_image_thumb.jpg?1604354463)
Perampanel as an AED
- non-competitive blockade of AMPA glutamate receptor
- release of glutamate cannot overcome the block
- reduce spread/generalisation of seizure
- can also affect behaviour and mood
What role or lack thereof does GABA play in the occurrence of a full-blown seizure?
- Focal epilepsy characterised by intermittent high amplitude discharges at site of epileptic focus during inter-ictal (seizure) periods.
- Two phases:
- synchronous depolarisation (caused by strong excitatory inputs to the region of the focus),
- followed by a period of hyperpolarisation, (activation of GABA inhibition)
- Transition from inter-ictal discharges to full-blown seizure is a decrease in the hyper-polarisation phase
- failure of inhibition to kick in, therefore treating with GABA stimulants helps control the seizure
What drugs enhance GABA-ergic synaptic transmission?
- sodium valproate (sodium channels)
- benzodiazepines (clobazam, lorazepam)
- barbiturates/ primidone pro drug
- tiagabine (inhibits GABA re-uptake)
- vigabatrin (inhibits GABA –T breakdown)
What is Levetiractem?
- high-affinity synaptic vesicle protein-2A ligand that modulates glutamate neurotransmitter release
- rapidly up titrated and is effective
- IV formulation; no drug-drug interactions
- keeps patients alert but causes mood lowering/agitation side-effects
- brivaracetam second-generation version
What drugs would be suitable for Primary Generalized Epilepsy?
First line
- Sodium valproate
- Lamotrigine
Second line
- levetiracetam, topiramate, zonisamide, benzodiazepines
What drugs would be suitable for Partial (focal onset) epilepsy?
First line
- Carbamazepine
- Lamotrigine
- all other AEDs have efficacy
Go over the toxicity effects of Benzodiazepines
Dose related (acute)
- Drowsiness
- Ataxia
- Hyperactivity
- cognitive impairment
Long term
- Tolerance/ Dependence
Go over the toxicity effects of Phenytoin
Dose-related (acute)
- Ataxia
- Diplopia
- Nystagmus
Long-term
- Gingival hyperplasia
- Osteomalacia
- Cerebellar atrophy
Go over the toxicity effects of Sodium Valproate
Dose-related (acute)
- Sedation
- Tremor
Long-term
- Hair thinning
- Weight gain
- Menstrual irregularities
- Encephalopathy
- Parkinsonism
(is an enzyme inhibitor)
Give an overview of the Motor Control of Hierarchy
- High for strategy: Association areas of Neocortex and basal ganglia
- Medium for tactics: Motor Cortex and Cerebellum
- Low for execution: Brainstem and Spinal Cord
Give an overview of the corticospinal tracts from the motor cortex to the skeletal muscles
![](https://s3.amazonaws.com/brainscape-prod/system/cm/389/120/719/a_image_thumb.jpg?1604046038)
rubro = red
Give an overview of the Rubrospinal tract
- predominentley innervates the flexor muscles in the upper limb
![](https://s3.amazonaws.com/brainscape-prod/system/cm/389/120/721/a_image_thumb.jpg?1604046209)
Give an overview of the Vestibulospinal tract
- originates in the vestibular nuclei of the medulla which relay sensory information from the vestibular labyrinth in the inner ear
- Medial Vestibulospinal pathway activates the cervical spinal circuits that control neck and back muscle guides
- guides head movements
- helps keep eyes stable as the body moves
- Lateral vestibulospinal projects ipsilaterally far down the lumbar spinal cord
- helos maintain an upright and balanced posture
- facilitates the extensor motor neurons of the legs
![](https://s3.amazonaws.com/brainscape-prod/system/cm/389/120/722/a_image_thumb.jpg?1604046698)
Give an overview of the Tectospinal tract
- Originates in the superior colliculus in the midbrain
- The superior colliculus receives information from the retina and the visual cortex used to construct the map of the world around us
- allows the direction of the head and eyes so that the appropriate point of space is imagined on the fovea
- The neurons decussate immediately and lie close to the midline into the cervical region of the spinal cord
- help control muscles of the neck, upper trunk and shoulder
Give an overview of the Reticulospinal tract
- Reticulospinal tract descends in two separate pathways
- Pontine (medial)
- Medullary (lateral)
- both facilitate the extension of the limbs
- the pathway runs from the brainstem, the reticular formation is under the cerebral aqueduct and fourth ventricle
![](https://s3.amazonaws.com/brainscape-prod/system/cm/389/120/724/a_image_thumb.png?1604047372)
What are the 5 descending pathways in the spinal cord
- Tectospinal and medial vestibulospinal
- Control head and neck movements.
- Lateral vestibulospinal and reticulospinal
- Activate extensor muscles in arms and legs.
- Rubrospinal
- Activates flexor muscles in arms.
Explain the meaning of different Posturing in Coma
-
Decorticate posturing: the lesion is above the red nucleus
- the rubrospinal neurons are disinhibited and therefore facilitate flexors in the upper limbs (lesions above the red nucleus)
- Decerebrate posturing: the rubrospinal neurons are disrupted and therefore upper limbs are extended (lesions below the red nucleus)
-
Noxious stimuli allow us to understand where the lesion is
- supraorbital pressure
- nail bed stimulation
- sternal stimulation
What is the impact of damage to the motor cortex and corticospinal tract
- loss of descending inhibition
- Typical Posture
- some preserved upper limb flexion
- lower limb extension
- Increased tone (spasticity),
- Brisk Reflexes:
- Extensor Plantar/Babinski reflex: abnormal extension of toes (up till age 2 is normal)
- Clonus
- Patient maintains a posture
What is the blood supply of the brain?
- Anterior Cerebral artery –> Frontal
- Middle Cerebral Artery –> Temporal and Parietal
- Posterior Cerebral Artery –> Occipital
- Anterior choroidal artery + Branch of Internal Carotid –> centre of the brain
![](https://s3.amazonaws.com/brainscape-prod/system/cm/389/120/728/a_image_thumb.png?1604058837)
What is the consequence of the middle cerebral artery occlusion?
- a Proximal lesion would affect the internal capsule
- leading to complete hemiparesis
- a Distal lesion may spare the leg area of the motor cortex
- (secondary swelling and ischaemia may compromise function)
What is the consequence of an Anterior Cerebral Artery stroke?
- this supplies the medial part of the frontal lobes including leg area of the motor cortex
- leg (crural) paresis
- frontal sing e.g abulia: loss or impairment of the ability to make decisions or act independently
What is a Jacksonian Seisxre (March)
- partial onset of a simple motor seizure becoming secondarily generalised
- strongly associated with a structural abnormality in or close to the motor cortex
![](https://s3.amazonaws.com/brainscape-prod/system/cm/389/120/731/a_image_thumb.png?1604059781)
What is the role of the Posterior Parietal Cortex?
- Area 5- somatosensory afferents
- Area 7- visual pathway afferents
- Mental body/ environment image
- Damage results in neglect (can perceive but do not attend)
- Exploratory movements
- Eg turning object in hand (looking and feeling)
![](https://s3.amazonaws.com/brainscape-prod/system/cm/389/120/732/a_image_thumb.jpg?1604059878)
What inputs allow for motor planning?
- Visual, Auditory, Somatosensory, Vestibular, Gustatory
all feed into the Heteronodal which allows for motor planning
- the prefrontal cortex plans for movement after receiving information from the other cortices in the brain
![](https://s3.amazonaws.com/brainscape-prod/system/cm/389/120/733/a_image_thumb.png?1604060089)
Give an overview of the Premotor Area (PMA)
- Importance in control of visually guided movements
- origination of the hand in relation to the object to be grasped (prehension)
- Damage: may cause perseveration of motor activity despite lack of success
- receives input from the cerebellum is involved in planning movements based on visual cues, mostly involved in
- control of postural and proximal limb muscles
- lesions in the PMA disrupts response to visual cues
What is Apraxia?
Inability to carry out purposeful movements in the absence of paralysis or paresis. There is great difficulty in the sequencing and execution of movements
-
Ideational (Parietal) apraxia: unable to report sequence
- show me how to make a peanut butter sandwich
-
Ideomotor (SMA) apraxia: unable to use the tool
- show me how to hold and use a pair of scissors
What is Dystonia?
Sustained muscle contractions, usually producing twisting and repetitive movements or abnormal postures or positions. If only occurs with certain actions, said to be ‘task specific’.
- though manifestation is motor, the primary abnormality is likely to be disrupted sensory processing mediated by the basal ganglia
What is the role of the Anterior Cingulate Gyrus
![](https://s3.amazonaws.com/brainscape-prod/system/cm/389/120/737/q_image_thumb.jpg?1604062392)
implicated in
empathy, impulse control, emotion, and decision-making
What is the role of the Basal ganglia
![](https://s3.amazonaws.com/brainscape-prod/system/cm/389/120/738/q_image_thumb.jpg?1604062522)
Positive feedback loop with the cortex to select wanted movements and deselect unwanted movements.
What is the function of the Cerebellum
- Coordination of muscles in order to make smooth movements.
- Balance
- Motor learning
- Cognitive functions
Recreate this sagittal section of the Cerebellum and the cerebellar peduncles
![](https://s3.amazonaws.com/brainscape-prod/system/cm/389/120/740/q_image_thumb.jpg?1604138143)
Gross anatomy of the cerebellum
![](https://s3.amazonaws.com/brainscape-prod/system/cm/389/120/742/a_image_thumb.jpg?1604138413)