Before the Exam Flashcards
what happens when there is damage to the premotor and supplementary motor cortex
- damage to areas 6 and 8 either medial or lateral lead to the clinical syndrome of motor apraxia
what does damage to the posterior parietal cortex do
sensory apraxia
what causes oculomotor apraxia
bilateral frontal field lesions
what happens if you have a lesion in the dorosolateral prefrontal cortex
- apathy
- personality changes
- lack of ability to plan or to sequence actions of tasts
- poor working memory for verbal information (if the left hemisphere has a lesion ) or spatial information (if the right hemisphere has a lesion)
What happens if you have damage to the orbitofrontal cortex
- Disinhibition of these drives after orbital damage leads to pseudopsychopathic behaviour
- This can be defined as impulsiveness, puerility, a jocular attitude, sexual disinhibition, and complete lack of concern for others.
- Patients with such acquired sociopathy, or pseudopsychopathic disorder, are said to have an orbital personality
where do the lateral cotricospinal tract and anterior cotricospinal tract run
Lateral corticospinal tract runs in the dorsolateral cord
Anterior corticospinal tract in medial ventral cord (only present in the cervical cord)
describe the lateral vestibulospinal tract
- origin
- where the nucleus projects
- what does it control
- Origins: vestibular nuclei in upper medulla/lower pons
- Nucleus projects ipsilaterally to antigravity muscles
- Tonically active during upright posture
- Controls posture and balance
describe the reticulospinal tract
- origin
- where the nucleus projects
- what does it control
- Arises in reticular formation of pons and medulla
- Projects diffusely (bilaterally) down spinal cord
- Responsible for autonomic control (drives sympathetic preganglionic neurones) also drive to respiration (phrenic nerve)
- General ‘arousal’ of spinal cord
describe the rubrospinal tract
- origin
- what does it do
- origin is the red nuclues in brainstem
- carries cerebellar commands to the spinal tract
- probably plays a role in control of movement velocity and transmitting motor commands from the cerebellum to the musculature
describe what the tectospianl tract do and where does it originate
- a pathway that cooridnates voluntary head and eye movement, it activates reflex movements of the head in response to visual and auditory stimuli
- originates in the superior collicus and projects to the contralteral cervical spinal cord to terminate in lamine VI, VII, VIII
describe upper motor neurones
- possible location
- common causes
- structures involved
- distribution
- voluntary movements
- muscle tone
- myotactic reflexes
- cutaneous relfexes
- muscle bulk
- classical description
- possible location - CNS only
- common causes - CVA, trauma, MS, ALS, infectious disease
- structures involved - Motor cortex or corticospinal tract
- distribution- never individual muscles, always group of muscles
- voluntary movements - paralysis or paresis especially of skilled movements
- muscle tone -increased, particularly in antigravity muscles
- myotactic reflexes - hyperactive or exaggerated
- cutaneous relfexes - some abnormalities e.g. positive babinski sign
- muscle bulk - may be slight atrophy
- classical description - spastic paralysis
describe lower motor neurone lesion
- possible location
- common causes
- structures involved
- distribution
- voluntary movements
- muscle tone
- myotactic reflexes
- cutaneous reflexes
- muscle bulk
- classical description
- possible location - CNS or PNS
- common causes- CVA, polio, tumour, trauma, alcoholism, diabetes
- structures involved - spinal or brainstem - motor neurones or peripheral motor axons
- distribution - segmental - limited to muscles innervated by damaged motoneurons or their axons
- voluntary movements - paralysis
- muscle tone - decreased
- myotactic reflexes - decreased or absent
- cutaneous reflexes - decreased or absent
- muscle bulk - pronounced atrophy
- classical description - flaccid paralysis
name the functional three zones in the cerebellum and what they comprise of
- Vestibulocerebellum comprises Flocculonodular lobe connected to lateral vestibular nucleus (in pons)
- Spinocerebellum comprises Anterior lobe and vermis connected to fastigial, globose & emboliform nuclei – connected to the spinal cord
- Cerebrocerebellum comprises Posterior lobe (cerebellar hemisphere) connected to dentate nucleus – connected to the cerebrum
what does the vestibulocerebelum do
- coordinates head and eye movement to ensure the stability of gaze
- controls balance of the head on the body via the medial vestibulospinal tract
- control the balance of the body on the ground via the lateral vestibulospinal tract
what does the spinocerebellum do
2) The Spinocerebellum (anterior lobe and vermis) controls locomotion and limb co-ordination:
- it sends motor commands down the reticulospinal tracts to co-ordinate postural and locomotor movement
what does the cerebrocerebllum do
- Co-ordinates movement initiated by motor cortex.
- This includes speech, voluntary movements of hands and arms, and hand-eye co-ordination.
describe flocculonodular syndrome
- Little control of axial muscles
- Wide-based ‘ataxic’ gait, reeling and swaying
- Tendency to fall to side of lesion
- Nystagmus
- Severe cases cannot sit or stand without falling
what are the symptoms of anterior lobe damage
Ataxia: ataxic gait (overlaps with flocculonodular syndrome) – widely spaced legs in order to keep balance
Hypotonia: generalised muscle weakness and fatigue,
Reflexes may be depressed or pendular (upper motor neurone lesions
what symptoms are in neocerebellar syndrime
Loss of hand-eye co-ordination.
Dysmetria (inaccurate reaching with intention tremor
Dysdiadochokinesis is the irregular performance of rapid alternating movements of hands
Intention tremors occur on an attempt to touch an object. A kinetic tremor may be present in motion. The finger-to-nose and heel-to-knee tests are classic tests of anterior lobe cerebellar dysfunction. 0inability to flex and extend easily?
Loss of good speech articulation (slurred speech) due to loss of co-ordination of muscles involved in speech production.
There may be a loss of cognitive eye movement (active scanning) and other perceptual difficulties or motor difficulties involving skilled movements (eg playing a muscial instrument)
There may also be deficits in selective attention& perception due to failure of ‘eye movement programs”
what gene defects can cause a life without pain
Loss of Tranduction/Transmission
Loss of NaV1.7
= (sodium channel subunit)
= Congenital indifference to pain
Loss of C fibres
= trkA - NGF receptor mutation
= Congenital insensitivity to pain with anhydrosis CIPA
what are the two types of C fibres
- ‘peptidergic’ C fibres release peptides peripherally e.g., Substance P / CGRP
= this leas to Vasoactive, promote inflammatory responses (neurogenic inflammation) and healing; thermal nociception - ‘Peptide-poor’ C fibres have distinct receptors (e.g., P2X3 ATP receptors) and projections
= these leads to mechanical nocicpetion
describe the pathway of the anterior spinothalamic (or neospinothalamic) tract
- Primary afferent: Aδ fibres as well as input from C (indirect via interneurons) and Aβ fibres innervate →
- Projection neurones in Lamina V – ‘wide dynamic range cells’. After decussating axons travel in the anterior spinothalamic tract
- innervate ventral posterior lateral (VPL) and ventral posterior medial (VPM) – somatosensory thalamus; and ventral posterior inferior (VPI) and central lateral (CL) nuclei of the thalamus (reticular and limbic associated areas).
- The main projection is to the primary somatosensory cortex (SI) from
VPL/ VPM →; localisation & physical intensity of noxious stimulus
- input to SII (secondary somatosensory cortex) via VPI
- and ACC (anterior cingulate cortex; emotion) and prefrontal cortex and striatum via CL (sites for cognitive function/ strategy)
describe the pathway of the lateral spinothalamic (or paleospinothalamic) tract
- Primary afferent: C fibres but also some Aδ fibres innervate →
- Projection neurones in Lamina I –After decussating axons travel in the lateral spinothalamic tract
- innervate the more posterior/ medial parts of the thalamus
Mediodorsal nucleus (ventrocaudal) (MDvc)
‘Posterior thalamus’ – posterior nucleus (medial subnucleus) (POm) and ventral medial nucleus (posterior) (VMpo)
(also some projections to the VPL, VPM and CL) - Projections to Cortex MDvc → anterior cingulate cortex (ACC); (emotion/ motivation) Posterior thalamus (POm and VMpo) → anterior or rostral insula (emotion, quality i.e. ‘pain’, autonomic integration)
describe the three other areas that the lateral spinothalamic tract project to
the limbic system
- subjective sensations of pain
- goes via the brainstem and posterior medial thalamus
Midbrain reticular formation
- pain - induced arousal and descending control of nociceptor input
Intralaminar(reticular) nuclei of thalamus
- alerting cerebral cortex and focus of attention of pain
How do prostaglandins lead to inflammatory pain
PGs sensitise C-fibres by increasing numbers of other receptors and increasing the number of open sodium channels. There are also central (i.e. spinal cord) sensitising effects
what causes the intensity of the pain
- superior parietal lobe and insula and amygdala pathway
What feeling causes the unpleasantness of pain
ACC - PFC - PAG path emotion/ placebo control– unpleasantness
How does PAG and the nucleus raphe Magnus inhibit pain
Electrical stimulation of PAG or NRM inhibits spinal thalamic cells, (i.e. spinal neurons that project monosynaptically to the thalamus) in laminae I, II and V so that the noxious information from the nociceptors are modulated at the spinal cord level
Electrical stimulation of the PAG elicits release of endorphin while stimulation of the NRM causes release of serotonin (5-HT).
What is the treatment for trigeminal neuralgia
Treatment = carbamazepine, baclofen, phenytoin, valproate, clonazepam, baclofen with carbamazepine
what are the other treatment options beyond drugs for epilepsy
Neuromodulation: vagal nerve stimulation, deep brain stimulation
Ketogenic diet (diet high in fat and low in carbohydrates, e.g. 4:1 ratio)
New anti-epileptic drugs: example of cannabidiol for treatment-resistant epilepsy
What are the three main areas in the brain that are important in chronic pain
- Sensory/discrimitive pain – localisation in time and space, assessment of intestine, lateral system, lateral thalamic nuclei S1, S2, SMA
- Affective/motivational – emotional/unpleasant aspects, reward in escape, medial system (HG medial thalamic nuclei, ACC, insula)
- Cogntivie/evaluative – interpretation of pain and its meaning, cogntivie system (ACC DLPC)
what can happen when MCA stroke occurs
– Dominant hemisphere(depends which hemisphere, tend to be the left hemisphere)
• Global aphasia (don’t understand and cant generate speech), can also have expressive and receptive aphasia if brocas or wernickes area is developed, – left hemisphere damage
• Sensorimotor loss on contralateral face, upper limb and trunk (for either left or right hemisphere)
– If it’s the Non-dominant hemisphere that is damaged
• Neglect syndrome
what happens in the anterior cerebral artery stroke
– Contralateral sensorimotor loss below waist – effects the medial wall, therefore effects below the waist
– Urinary incontinence
– Personality defects – if in the frontal lobe
– Split-brain syndrome
What are the effects of the posterior cerebral artery stroke
– Contralateral homonymous hemianopsia
– Reading and writing deficits
– Impaired memory (memory is in the temporal lobe which is largely supplied by PCA)
What are the symptoms of TIA in
- anterior circulation
- posterior circulation
– Anterior circulation
• Motor weakness
• Hemi-sensory loss
• Dysarthria - difficult or unclear articulation of speech
• Transient monocular blindness – if ophthalmic artery
– Posterior circulation • Vertigo • Diplopia • Ataxia • amnesia
describe the characteristic of an epidural (extradural) haematoma
– Traumatic
– Blood between dura mater and the skull
– Bleeding rapid (arterial*)
– 2.7-4% of Traumatic brain injury
– Mortality 10% if they are caught early – person seems fine and the next minute they have collapsed
describe the characteristics of a subdural haematoma
– Traumatic / Ageing(Chronic)
– Blood between dura mater and arachnoid mater – pushing onto the brain surface
– Rupture to bridging veins – therefore they tend to be venous drainage that has been affected
– These spread more
– Acute 12-29% of severe TBI
– Mortality 40-60%
describe the characteristics of a subarachnoid haematoma
– Spontaneous – Between arachnoid and pia – Ruptured aneurysm or head injury – 1-7% of strokes – Arterial – Most frequent traumatic brain lesion
what are the symptoms of a subdural haematoma
– Irritability – Seizures – Headache – Numbness – Disorientation
What are the symptoms of extradural (epidural) haematoma
– As blood collects it compresses intracranial structures
– Compress cranial nerve III
– Weakness of extremities on opposite side of lesion (crossed pyramid pathways)
– Loss of visual field opposite to lesion (compress of PCA)
What are the symptoms of a subarachnoid haematoma
• Symptoms
- Severe headache (thunderclap) due to compression of the brainstem and confusion and fluctuations of consciousness
–
– Vomiting
– Confusion
– Lowered / fluctuating levels of consciousness
how do you administer gepants v monoclonal abs
Gepants - oral
Monoclonal abs - IV/SC
describe how operant conditoning can lead to drug addiction
Behaviour leading to a central reward (one candidate is dopamine release in the core of nucleus accumbens) gets activated in circumstance in which the reward was attained with the same behaviour previously - example of operant conditioning as person gets a reward for their behaviour therefore they are more likely to do it again
name the positive reinforcement involved in drug use
Pleasurable sensation
Satisfaction of biological needs (e.g. cocaine and nicotine reduce hunger)
Social reinforcement, e.g. group membership
name the negative reinforcements involved in drug use
Reduction of habitual stress level
Reduction of acute distress
Increased pain threshold
Reduction of withdrawal symptoms
describe sensitivity to negative drug effects
Biological sensitivity to drug after-effects (hang-over)
Intensity of withdrawal discomfort
Reactions to withdrawal discomfort
describe Sensitivity to positive drug effects
Sensitivity to drugs (genetic/biological factors, but also expectancies)
High habitual stress levels
Absence of other sources of gratification
What is currently NICE approved for deep brain stimulation
- Parkinson’s disease (hypokinetic movement)
- essential tremor (hyperkinetic movement)
- dystonia (hyperkinetic movement)
describe and name the different types of tremor
there are two main categories these are resting tremor and action tremor
Resting Tremor
- this is when you have a tremor while resting
Action tremor
- either postural, kinetic and intention
- a postural tremor is a tremor when you life a limb such as an arm - holding something against gravity
- Kinetic - occurs with voluntary movement
- Intention - occurs with goal directed movement and worsens as approaching the target
Describe the neuronal connections in the limbic system
- Information goesfrom the cingulate cortex to the parahippocampal gyrus
- Information goes from the parahippocampal cortex to the hippocampus
- Information goes from the hippocampus along the fornix to the mamillary bodies of the hypothalamus
- Information goes from the hypothalamus to the anterior thalamus
- Information goes from the anterior thalamus back to the cingulate cortex
what is kluver bucy syndrome and what are the symptoms
- this is when the subject loses all sense of fear
symptoms
- Psychic blindness (inability to process information).
- Oral tendencies.
- Hypermetamorphism; grabbing objects in view and appropriately using them-
but not at appropriate times.
- Altered sexual behaviour.
- Emotional changes.
Describe the pathway of the amygdala
- Septal nuclei is a sensory mechanism, which connects to the reticular formation.
- The RF forwards the signal to the ventral striatum (nucleus accumbens).
- The signal is sent to the amygdala where it can activate fight or flight.
- The commands are sent to the hypothalamus, which is then sent again to the RF.
- The reticulospinal tracts can then be activated and a response triggered.
What do plaques and tangles cause to happen
- neurotic dystrophy
- synaptic loss
- selective neuronal cell loss
what are the side effects of memantine
- less common and less severe than the cholinesterase inhibitors side effects; - dizziness - headahces - tiredness - increased blood pressure - constipation
What are the symptoms of addiction
Bingeing, having loss of control.
Withdrawal.
Cravings.
Intoxifiacation.
describe the mechanism of action underlying withdrawal symptoms
- the ventral tenemental area releases dopamine that will stimulate the dopamine receptors
- neurones receive that input and project back releasing GABA and dynorphin which stimulate Kappa receptors
- Dynorphin will have an inhibitor effect on the VTA neurone and will trigger an unpleasant feeling so in order to get more reward again you need to stimulate it with the drug again
