Brain + Behaviour wk3+4 Flashcards
Which tract does the insula receive projections from?
the insula receives projections from the lateral spinothalamic tract. This pathway is primarily responsible for the conduction of information regarding pain, and temperature.
After reaching the ventral posterior lateral thalamus, projections from the lateral spinothalamic tract go to the cerebral cortex specifically the anterior cingulate cortex and insula. This generates the sensation of pain and interpreting its emotional meaning.
Describe what the limbic system is made up of and what it’s function is
The limbic system is a complex set of brain structures associated with emotional processing, memory, and motivation
the limbic system includes the hippocampus, amygdala, hypothalamus, and cingulate cortex
Describe the reward system + demonstrate how it is involved in motivation + reinforcement learning
Brain’s Reward System:
Components: Includes structures such as the nucleus accumbens (NAc), ventral tegmental area (VTA), and prefrontal cortex.
Function: Regulates feelings of pleasure, motivation, and reinforcement learning by processing rewarding stimuli.
Role of the Nucleus Accumbens (NAc):
Location: Situated in the basal forebrain, part of the ventral striatum.
Function in Motivation: Acts as a central hub for processing rewards, influencing motivation to engage in goal-directed behaviors.
Function in Reinforcement Learning: Encodes reward prediction and outcome, facilitating learning from experiences to repeat rewarding actions.
Mechanism:
Rewarding stimuli trigger dopamine release from the VTA to the NAc.
This dopaminergic activity reinforces behaviors, enhancing the likelihood of repetition.
Research Insight:
Studies indicate that different subregions of the NAc contribute distinctly to reward-related behaviors, highlighting its complex role in motivation and reinforcement learning
Rabies notoriously makes people abnormally aggressive. What area of the brain is damaged in patients with rabies?
hippocampus, brainstem, thalamus + spinal cord
can you give the region associated with each of the following emotions:
- arousal
- happiness
- sadness
- fear
- anger
- disgust
- arousal= amygdala
- happiness= dorsal anterior cingulate
- sadness= subgenual anterior cingulate
- fear= amygdala
- anger= orbitofrontal cortex
- disgust= anterior insula
What is the Moro reflex + what age does it disappear
The Moro reflex is a fast reflex response elicited by a sudden loss of support that is found in young infants + disappears between 3-6 months of age
what is the acoustic startle reflex
The acoustic startle reflex is an extremely fast defensive response to an unexpected loud noise aimed at protecting the back of the neck and the eye (eyeblink) + does not disappear with age
What is Urbach-Wiethe disease?
Urbach-Wiethe disease is a rare recessive condition that causes calcium to build up into the amygdala until it wastes away
symptoms:
- Beading of the papules around the eyelids
- fearless (they feel angry not afraid when being robbed)
- they can feel everything but fear
What are some essential features of anxiety disorders
features of anxiety disorders:
- excessive + enduring fear
- anxiety or avoidance of perceived threats
- can include panic attack
Explain which regions are hyperactive in
- PTSD
- panic disorder
- social phobia
- specific phobia
PTSD=
hyperactive: amygdala, dACC, insular cortex
hypoactive: vmPFC, hippocampus
panic disorder=
hyperactive: amygdala, brainstem + dACC as well as reduced grey matter volume
hypoactive
social phobia= hyperactive amygdala
specific phobia= hyperactive amygdala, dACC, insular cortex
Alzheimer’s disease is associated with loss of _____ in the ___ ____
Alzheimer’s disease is associated with loss of cholinergic neurons in the basal forebrain.
Multiple Sclerosis is associated with loss of _____
Multiple Sclerosis is associated with loss of oligodendrocytes.
Huntington’s disease is associated with loss of ____ _____ ______-
Huntington’s disease is associated with loss of striatal (corpus striatum) medium spiny neurons.
what is the striatum made up of?
the striatum is a major component of the basal ganglia (forebrain nuclei) and is composed of the nucleus accumbens, the olfactory tubercle, and the caudate nucleus and putamen
What regions of the brain are hyperactive vs hypoactive in Major Depressive Disorder (MDD) and Substance Use Disorder (SUD)
MDD Hyperactive: Amygdala, sgACC, Lateral OFC
MDD Hypoactive: dlPFC, Striatum/Nucleus Accumbens
SUD Hyperactive: Amygdala, mPFC
SUD Hypoactive: dlPFC, ACC
what does a pronator drift indicate?
a pronator drift might be a sign of corticospinal lesion opposite to the arm with the pronator drift
(upper motor neuron lesion sign; commonly seen after stroke)
What frequency tuning fork do you use for:
- neurological exam to test for vibration
- Rinne’s + Weber’s
neurological exam to test for vibration= 128Hz (longer one)
Rinne’s + Weber’s= 512Hz (smaller)
What is a positive Rombergs test? And what does it indicate
Positive Romberg= good balance when eyes open, but lose balance when closing their eyes
indicates problem with proprioception or vestibular function
The biceps reflex tests for which spinal roots?
C5/6
A change in the biceps reflex indicates pathology at the level of musculocutaneous nerve, segment C5/6 or at some point above it in the spinal cord or brain.
The triceps reflex tests for which spinal roots?
C7/8
The triceps reflex, a deep tendon reflex, is a reflex that elicits involuntary contraction of the triceps brachii muscle. It is sensed and transmitted by the radial nerve. The reflex is tested as part of the neurological examination to assess the sensory and motor pathways within the C7 and C8 spinal nerves
What does the brachioradialis reflex test for?
The brachioradialis tendon is used clinically to test C6 spinal nerve root. Which is affected in C5-C6 disc herniation.
You ask a patient to alternate clapping with front and back of hand when you’re testing their upper limb for co-ordination. If they struggle what is this called?
If patient struggles with alternating clapping (when you test for coordination) it’s called DYSDIADOCHOKINESIA (the inability to perform rapid alternating muscle movements)
What does the heel-shin test examine? and if patient can’t what does it indicate
the heel-shin test is a part of the neurological examination of co-ordination: the patient runs the sole of one foot up and down the shin of the opposite leg. if cerebellar disease is present, then the test is performed poorly and intention tremor may become pronounced
What nerve root does the Achilles tendon reflex test for?
S1/S2
The LMN of the Achilles reflex consists of the ventral horn of the S1/S2 nerve roots and the tibial nerve
to perform it:
- hold sole of foot and tap the thickest part of tendon
- watch for plantar flexion against your hand (caused by contraction of gastrocnemius muscle)
To test for plantar reflex you can scrape lateral side of foot with blunt instrument or thumb. What would be a normal response and what would be pathological?
normal response= big toe plantarflexion
pathology= +ve BABINSKI SIGN; big toe dorsiflexes (goes up) indicative of UMN lesion (n.b. might be normal up until 2yrs of age/norm bby reflex)
increased tone/hypertonia is as a result of what type of lesion?
decreased tone/hypotonia is as a result of what type of lesion?
increased tone/hypertonia is as a result of Upper motor neurone/UMN lesion
decreased tone/hypotonia is as a result of Lower motor neuron/LMN lesion
what’s the difference between spasticity + rigidity
spasticity= depends on speed; tone increases with speed of movement
rigidity= does NOT depend on speed; tone is stable with speed + doesn’t depend on direction of movement
In chronic cocaine users, what receptor has reduced availability/ what brain changes in cocaine use
In cocaine abusers the availability of dopamine D2 receptors + reduced cortical metabolism
Structural Brain Changes: alterations in the prefrontal cortex, such as reduced grey matter volume= linked to impairments in decision-making, impulse control, and increased susceptibility to relapse.
ΔFosB is a truncated splice variant of the Fos family transcription factors.
Unlike c-Fos, which degrades quickly, ΔFosB is stable and accumulates with repeated drug exposure.
It remains active for weeks after drug use stops, making it a key molecular marker of addiction. Explain the role of FosB and its effect on gene expression
ΔFosB = Stable transcription factor in addiction.
Accumulates with repeated drug use.
Persists long after drug use stops.
Increases drug sensitivity & reinforces addiction.
Modifies gene expression in the nucleus accumbens.
Chronic abuse of alcohol leads to significant neuroadaptations, altering brain structure and function. Explain some of these changes.
Alcohol:
- Neurodegeneration and Cognitive Impairment: Prolonged alcohol consumption can cause neurodegeneration, particularly in the medial prefrontal cortex (mPFC), leading to cognitive impairments.
- Thiamine Deficiency: Chronic alcohol use often results in thiamine (vitamin B1) deficiency, contributing to neurological disorders like Wernicke–Korsakoff syndrome, characterized by severe memory deficits.
Chronic abuse of morphine and/or heroin leads to significant neuroadaptations, altering brain structure and function. Explain some of these changes
Morphine and Heroin (Opioids):
- Neuroinflammation and Metabolic Dysregulation: Chronic morphine exposure induces neuroinflammation and disrupts glycolytic metabolism in the nucleus accumbens (NAc), a key region in the brain’s reward system.
- Altered Neuronal Physiology: Long-term opioid use leads to changes in neuronal function within the NAc, affecting reward processing and reinforcing addictive behaviors.
- What are the MDMA cellular targets?
- Chronic abuse of MDMA leads to significant neuroadaptations, altering brain structure and function. Explain some of these changes
1.MDMA cellular targets:
- 5-HT uptake system
- dopamine uptake system
- 5-HT2 receptors
- H2 histamine receptors
- alpha2 adrenergic receptors
- MDMA (Ecstasy):
- Serotonergic Neurotoxicity: Repeated MDMA exposure can damage serotonergic neurons, leading to long-term deficits in mood regulation and memory.
- Cognitive Impairments: Users may experience persistent cognitive deficits, particularly in memory and executive function.
Acute MDMA toxicity causes the following:
- temperature elevation
- disseminated intravascular coagulation (widespread clotting all over body)
- increased renal reabsorption of water
- hyponatraemia
- cerebral oedema
What is Rhabdomyolosis and what drug blocks it?
Rhabdomyolysis is a serious (potentially) life-threatening condition; when damaged skeletal muscle breaks down rapidly, releasing myoglobin into blood.
This can lead to severe complications, including kidney failure, electrolyte imbalances, and cardiac arrhythmias
symptoms of Rhabdomyolosis:
✅ Muscle pain, swelling, and weakness
✅ Dark, cola-colored urine (from myoglobin)
✅ Extreme fatigue or confusion
✅ Nausea, vomiting
✅ Irregular heartbeat (due to electrolyte changes)
Rhabdomyolosis is blocked by dantrolene (a muscle relaxant primarily used to treat malignant hyperthermia but works for rhabdomyolosis)
Dantrolene directly inhibits calcium release from the sarcoplasmic reticulum (SR) in skeletal muscle by blocking the ryanodine receptor (RyR1). This:
✔ Reduces excessive muscle contraction
✔ Decreases ATP consumption, preventing further muscle breakdown
✔ Limits heat and metabolic damage in conditions like malignant hyperthermia & neuroleptic malignant syndrome
Treatment of alcohol addiction (NICE)
- diazepam or chlordiazepoxide for detoxification (get them out of withdrawal)
followed up with one of the following to reduce cravings:
- acamprosate
- naltrexone
- disulfiram
- nalmefene
What opioid agonists and opioid antagonists commonly used to treat opiate addiction?
opioid AGONISTS; methadone (mu opioid agonist) and buprenorphine (partial mu opioid receptor agonist + kappa receptor antagonist; can also be used as transmucosal preparations) suppresses withdrawal symptoms + relieves craving
opioid antagonist; naltrexone (used after detoxification) ; has longer half-life than naloxone
Nicotine replacement therapy via gum, patch, sprays and inhalers is well known. What 2 medications (prescription only) are used to treat nicotine addiction
Bupropion= antidepressant; inhibitor of dopamine reuptkae
Varenicline= alpha4beta2 subtype selective partial agonist at nicotinic receptors); they help prevent relapse in people trying to quite
Pharmacological management of depression according to NICE
✅ First-Line SSRIs
1️⃣ Sertraline – Preferred due to low risk of drug interactions.
💊 Typical Dose: 50–200 mg/day
2️⃣ Fluoxetine – Often used, especially in younger patients.
💊 Typical Dose: 20–60 mg/day
3️⃣ Citalopram – Well-tolerated, but monitor for QT prolongation.
💊 Typical Dose: 20–40 mg/day (max 20 mg in elderly)
4️⃣ Escitalopram – Similar to citalopram, but with fewer side effects.
💊 Typical Dose: 10–20 mg/day
5️⃣ Paroxetine – Effective but may cause more withdrawal symptoms.
💊 Typical Dose: 20–50 mg/day
🧩 Alternative First-Line Options (If SSRIs Are Unsuitable)
🔹 Serotonin-Norepinephrine Reuptake Inhibitors (SNRIs)
Venlafaxine (Monitor blood pressure) – 💊 75–375 mg/day
Duloxetine (Useful for comorbid pain) – 💊 30–120 mg/day
🔹 Noradrenergic & Specific Serotonergic Antidepressant (NaSSA)
Mirtazapine – Good for sleep disturbances and appetite stimulation, but may cause weight gain.
💊 Typical Dose: 15–45 mg/night
🔹 Melatonergic Antidepressant
Agomelatine – Regulates sleep; monitor liver function.
💊 Typical Dose: 25–50 mg/night
⚠️ Key Considerations
SSRIs are first-line due to better safety and tolerability.
Mirtazapine or SNRIs may be used if SSRIs cause intolerable side effects.
Full effect takes 4–6 weeks; continue for at least 6 months after remission to prevent relapse.
Monitor for side effects: nausea, headache, sexual dysfunction, insomnia (SSRIs), or sedation/weight gain (Mirtazapine).
📝 Quick Recall:
✅ First-line = SSRIs (Sertraline, Fluoxetine, Citalopram, Escitalopram, Paroxetine)
✅ Alternative = SNRIs (Venlafaxine, Duloxetine), Mirtazapine, Agomelatine
✅ Monitor QT interval (Citalopram), Blood Pressure (Venlafaxine), Liver Function (Agomelatine)
What drug class are the following and how do they work: Clomipramine, imipramine, desipramine, amitriptyline
Tricyclic Antidepressants (TCAs) are the oldest antidepressants we have.
- Inhibit reuptake of amines
- Different degree of selectivity for amines (5-HT vs. noradrenaline) between them
- Have affinity for H1, muscarinic, α1 and α2 adrenoceptors
- Dangerous in overdose (cardiotoxicity)
- Adverse effects: dry mouth, blurred vision, constipation, urinary retention, aggravation of narrow angle glaucoma, fatigue, sedation, weight gain, postural hypotension, dizziness, loss of libido, arrhythmias
What drug class are the following and how do they work: Sertraline, Citalopram, escitalopram, fluoxetine, paroxetine
Selective Serotonin Reuptake inhibitors= inhibit serotonin transporter (SERT), reducing reuptake of serotonin + increasing serotonergic transmission
Adverse effects: nausea, headaches, gastrointestinal problems, increased aggression, insomnia, anxiety, sexual dysfunction
What drug class are the following and how do they work: Phenelzine, tranylcypromine
MONOAMINE OXIDASE INHIBITORS
Phenelzine, tranylcypromine (both inhibit MAO-A and MAO-B)- Irreversible inhibition of the enzyme (monoamine oxidase), enzyme which breaks down key neurotransmitters involved in mood regulation.
Moclobemide= reversible inhibition of MAO-A only
MAO-A: Breaks down serotonin (5-HT), norepinephrine (NE), and dopamine (DA).
MAO-B: Primarily metabolizes dopamine (DA) and phenylethylamine (PEA).
- Interactions with tyramine-containing food (mature cheese, pickled fish and meat, red wine, beer, broad bean pods, yeast extract)- restrictions continue at least 2 weeks after discontinuation
- Interaction with pethidine and sympathomimetic compounds
- Hepatotoxicity
- Treatment of atypical depression (with anxiety, phobia and hypochondria)
Escitalopram (SSRI) is an S isomer of which drug?
Escitalopram is an S-isomer of citalopram (both SSRIs)
what is the difference between
- antidepressant drug discontinuation syndrome
- serotonin syndrome
antidepressant drug discontinuation syndrome: It can occur after a decrease in the dose of drug taken, an interruption of treatment
or abrupt cessation of treatment; can be prevented by a very gradual discontinuation of treatment,
by using a very slow tapering of the doses taken. Commonly used antidepressants such
as paroxetine and venlafaxine, are more likely to be associated with withdrawal symptoms. It presents
with insomnia, anxiety, nausea, headaches, electric shock sensation, agitation, mood swings,
diarrhoea/abdominal cramps.
serotonin syndrome; This is a relatively uncommon adverse drug reaction caused by excessive central and peripheral serotonergic activity.It presents with neuromuscular hyperactivity (tremor, hyperreflexia, myoclonus, rigidity), autonomic dysfunction (tachycardia, blood pressure changes, hyperthermia,
sweating, shivering, diarrhoea), and altered mental state (agitation, confusion, mania).
Classical Conditioning is a type of learning where an irrelevant (neutral) stimulus acquires the property of a relevant stimulus e.g. when u ring a bell a untrained dog will not salivate, but a dog conditioned to eat after bell ring will salivate at the bell ringing not the sight of food
Define the following terms used in classical conditioning:
- conditioned stimulus (CS)
- unconditioned stimulus (US)
- unconditioned response (UR)
- conditioned response (CR)
- conditioned stimulus= previously neutral/irrelevant stimulus (bell)
- unconditioned stimulus= stimulus that elicits response (sight of food)
- unconditioned response= response that doesn’t have to be learned (salivation)
- conditioned response= learned response initiated by conditioned stimulus (salivating in response to bell ringing not the sight of food)
what muscle relaxant is used in electroconvulsive therapy (ECT)
Succinylcholine is the preferred muscle relaxant for ECT
It is a depolarizing neuromuscular blocker and is given in doses of 1 mg/kg to produce adequate muscle relaxation for intubating conditions within 30 seconds of administration.
Define these basic principles of classical conditioning:
- acquisition
- extinction
- savings
- spontaneous recovery
Acquisition – learning phase during which the CR strengthens, and therefore the occurrence of the response increases
Extinction – gradual weakening of the tendency to produce the CR
When there is multiple presentations of the CS not followed by the US
Savings – even after complete elimination of a CR, a substantial residual of the original learning is saved
Extinction is not unlearning
Spontaneous recovery –Partial recovery of a conditioned response, without any environmental prompting
When a response has been extinguished, but after a rest extinction trials are resumed
what therapy works by exposing the patient directly to their worst fears?
flooding/ implosion therapy
Aversion therapy; involves conditioning the patient to experience negative feelings in the presence of a new stimulus (e.g., electroshocks, nauseating drugs)
e.g. alocoholic is taught to see alcohol as a drug that makes him puke straight away instead of having a good time (the new stimulus wld be disufiram). What type of conditioning is aversion therapy?
Counterconditioning – the positive association between the unconditioned stimulus (US) and conditioned stimulus (CS) is replaced with a negative one
Explain the difference between classical conditioning and operant conditioning
Classical Conditioning:
- a reflexive/unconscious response
- environment controls the behaviour
- the response is not maintained by its consequences
Operant Conditioning:
- a complex voluntary behaviour
- the individual operates on environment
- the response is maintained or changed by its consequences
Operant conditioning is a type of learning where behaviour is influenced by rewards or punishments. Define the following terms used in operant conditioning:
- fixed ratio
- variable ratio
- fixed interval
- variable interval
Fixed Ratio – reinforcement is given after every Nth response
Variable Ratio – the rate of reinforcement is not stable
Fixed Interval – a certain time must pass before getting reinforcement
Variable Interval – time interval varies before getting reinforcement
What is positive punishment vs negative punishment
positive punishment= application of negative stimuli e.g. being hit, laughed at, poor grade
negative punishment= the removal of a pleasant stimulus e.g. restricted from enjoyable activities, like not being able to watch tv, go out etc.
What is the triad of core symptoms in schizophrenia; what is the average age of onset in males vs females
Schizophrenia is a chronic mental disorder characterized by a triad of core symptoms.
1) Positive symptoms: hallucinations, delusions, agitation, disorganised thinking, feelings of persecution
2) Negative symptoms: introversion, apathy, low self-esteem, personal neglect, affective flattening, avolition (a lack of motivation or reduced drive to complete goal-directed activities)
3) Cognitive symptoms: poor memory (working memory is particularly effected), attention deficit, executive dysfunction
average age disease onset:
males= 18-25 years
females= 25-35 years
what do we mean by ‘working memory’
Working memory= a type of short-term memory; it is a set of cognitive processes that allow us to store + manipulate temporary info
It’s like your brain’s notepad—it holds onto information for a short time while you’re using it.
For example:
When you do math in your head, like 23 + 47, your working memory holds the numbers while you calculate
When you hold a sentence in your mind to understand its meaning, your working memory is at work.
what is ‘affective flattening’ in schizophrenia and is it a positive, negative or cognitive symptom?
A flat affect can be a negative symptom of schizophrenia, meaning that your emotional expressions don’t show outwardly. You may speak in a dull, flat voice and your face may not change. You also may have trouble understanding emotions in other people.
what structural + functional changes are seen in the brain of a patient with schizophrenia
- larger ventricles
- smaller temporal lobes
- 2% reduction in brain volume
Schizophrenia is also associated with decreased synaptic spines + decreased dendritic complexity in the cortex
major neurotransmitters affected:
- striatum (increased dopamine + glutamate)
- frontal cortex (decreased grey matter, glutamate, dopamine, GABA, synaptic markers)
- temporal cortex (decreased grey matter volume)
what pathways in schizophrenia are hyperactive vs hypoactive
Schizophrenia is associated with a dual dopaminergic imbalance
hyperactive stritatum (mesolimbic pathway– ventral striatum + also in dorsal striatum)
hypoactivity in the mesocortical pathway– frontal cortex
Many antipsychotic drugs such as Haloperidol, Chlorpromazine, Fluphenazine, Trifluoperazin (typicals) and Risperidone,
Paliperidone (active metabolite of risperidone)
Amisulpride (atypicals) can cause sexual dysfunction, galactorrhoea, amenorrhea. An increase in what hormone causes this?
these antipsychotics cause a rise in prolactin = sexual dysfunction, galactorrhoea, amenorrhea
Effects of High Prolactin (Hyperprolactinemia)
Women: Irregular periods, amenorrhea, infertility, galactorrhea (milk production without pregnancy)
Men: Erectile dysfunction, low libido, gynecomastia (breast growth)
Both: Bone loss (osteoporosis) if prolonged
60% of D2 receptor occupancy is required for antipsychotic efficacy; if >80% D2 receptors are blocked theres a risk of EPS. What is EPS?
EPS= Extrapyramidal symptoms, this includes:
acute dystonias= Sudden, involuntary muscle contractions causing abnormal postures, often triggered by antipsychotic drugs.
parkinsonism= Movement abnormalities like slow movement, muscle rigidity, and tremors, resembling Parkinson’s disease. Can be medication-induced.
tardive dyskenesia= Involuntary, repetitive movements (especially facial) due to long-term antipsychotic use. Affects 20-30% of chronic schizophrenia patients
what is the first-line treatment for schizophrenia?
atypical antipsychotics are first-line
Neuroleptic malignant syndrome is a rare complication of antipsychotics. What is it?
Neuroleptic malignant syndrome (usually higher risk with typical antipsychotics) is a potentially lethal complication.
Symptoms:
- hyperpyrexia= extremely high fever (above 41°C)
- muscle rigidity
- tremor
- confusion
- autonomic instability
occurs up to 2-3% of patients taking antipsychotics
Anterior choroidal artery syndrome
the anterior choroidal artery also supplies the limbic system, basal ganglia, thalamus, and optic tract and radiation. Isolated occlusion of the AchA, results in Anterior choroidal artery syndrome which is characterised by the triad of
· Contralateral Hemiplegia
· Contralateral Hemianaesthesia
· Contralateral Hemianopia
what is the Griffiths III test
Griffiths III provides an overall measure of a child’s development, as well as an individual profile of strengths and needs across five areas:
Foundations of Learning – assesses critical aspects of learning during the early childhood years.
Language and Communication – measures overall language development, including expressive language, receptive language and use of language to communicate socially with others.
Eye and Hand Coordination – considers fine motor skills, manual dexterity and visual perception skills.
Personal–Social–Emotional – measures constructs relating to the child’s developing sense of self and growing independence, interactions with others, plus many aspects of emotional development.
Gross Motor – assesses postural control, balance and gross body coordination, among other abilities.
Kwashiorkor and Marasmus are outdated terms for severe acute malnutrition with or without oedema. Explain the difference between these
kwashiorkor (with oedema) is predominantly a protein deficiency, while marasmus (without oedema) is a deficiency of all macronutrients — protein, carbohydrates and fats
Kwashiorkor (SAM with Oedema)
Cause: Primarily due to protein deficiency, often with sufficient calorie intake.
Symptoms:
Generalized pitting oedema (fluid retention, especially in legs and feet)
Distended abdomen (due to fluid retention and fatty liver)
Skin lesions (dermatosis, peeling, darkened or lightened patches)
Hair changes (thin, brittle, discolored)
Apathy, irritability, and lethargy
Enlarged liver (hepatic steatosis)
Pathophysiology:
Reduced albumin levels lead to oedema.
Oxidative stress and gut dysbiosis contribute to the disease.
Marasmus (SAM without Oedema)
Cause: Severe calorie and protein deficiency (overall energy deficit).
Symptoms:
Severe wasting (muscle and fat loss)
No oedema
Thin, wrinkled skin
Extreme weakness and irritability
Sunken eyes, prominent bones
Growth retardation
Pathophysiology:
Body depletes fat stores and then breaks down muscle for energy.
Metabolic adaptation to starvation.
The spinal cord develops from the neural tube which typically closes between day 17-30 after conception. High maternal serum alpha-fetoprotein (AFP) can indicate spina bifida (a birth defect where a baby’s spine and spinal cord don’t develop properly, leaving a gap in the backbone; as the neural tube, which forms the brain and spine, doesn’t close completely. What are the 3 types of spina bifida and what is the most common cause?
Types:
Spina Bifida Occulta – Mildest form, hidden, no symptoms.
Meningocele – A fluid-filled sac forms outside the spine.
Myelomeningocele – Most severe; spinal cord and nerves are exposed, causing disability.
most common cause is vitamin B9/folic acid deficiency
The most common of these is the Chiari II malformation (Myelomeningocele type) in which the cerebellum is pulled to the rear of the fetal skull= causes breathing, swallowing + coordination issues
what is cretinism
Cretinism is a condition caused by severe hypothyroidism (low thyroid hormone levels) in infancy or early childhood, leading to stunted physical and mental development. It is now called congenital hypothyroidism and can be prevented with early treatment.
Causes:
Iodine deficiency (most common worldwide)
Thyroid gland defects (absent, underdeveloped, or non-functioning)
Genetic disorders affecting thyroid hormone production
what is neurotropism
Neurotropism (neuroinflammation + neuronal
damage by crossing blood-brai barrier) refers to the tendency of certain viruses, bacteria, or toxins to target and infect nerve cells (neurons).
Rabies virus → Infects the central nervous system (CNS), causing fatal encephalitis.
Herpes simplex virus (HSV-1 & HSV-2) → Can cause encephalitis or recurrent infections.
Poliovirus → Attacks motor neurons, leading to paralysis.
Varicella-zoster virus (VZV) → Causes chickenpox and later shingles in nerves.
what gait do patients with spastic cerebral palsy have
True Equinus. When the younger child with bilateral cerebral palsy begins to walk with or without assistance, calf spasticity is frequently dominant, resulting in a `true equinus’ gait with the ankle in plantar flexion throughout the stance and the hips and knees extended.
✔ Toe walking – The child walks on their toes with the heel off the ground.
✔ Ankle plantarflexion – The foot remains pointed downward due to tight gastrocnemius and soleus muscles.
✔ Knee and hip extension – The knees and hips remain relatively straight.
MRIs of the ADHD (inattention, hyperactivty, impulsivity) show what changes?
- increased grey matter volume
- loss of cortical thickness
Physical withdrawals from a drug are usually around 2wks, what are the symptoms the patient will experience when coming off the following:
- opiates
- barbiturates
- alcohol
- benzodiazepines
Opiates;
- nausea/vomiting
- hypertension
- anxiety/agitation
Barbiturates;
- sweating
- tremors
- delirium tremens
- anxiety/agitation
Alcohol
- delirium tremens
- sweating tremors
- anxiety/agitation
Benzodiazepines;
- convulsions
- panic attacks
- anxiety/agitation
Delirium tremens
Confusion. Severe autonomic hyperactivity such as trembling, sweating, tachycardia, nausea, and vomiting. Impaired consciousness. Visual, tactile, or auditory hallucinations
What causes acute tolerance/tachyphlaxis
acute tolerance/tachyphlaxis is a short lasting tolerance which occurs when a drug acts at a receptor which becomes desensitised at the first dose
Desensitisation/tachphlaxis causes acute tolerance
n.b. the diminishing effect of nicotine on changes in heart rate during the smoking day is an example of acute drug tolerance
What is pharmacokinetic tolerance
Pharmacokinetics (what does body do to the drug)
Pharmacokinetic tolerance= usually due to an increase in the metabolism of the drug caused by an induction of liver enzymes responsible for its degradation, and results in diminished response per dose of drug
this type of tolerance can be overcome by taking larger and larger doses of the drug
e.,g. barbituate tolerance= is due to drug-evoked induction of cytochrome P450 enzymes in liver= results in faster metabolism of barbiturates
difference between pharmacokinetic vs cellular tolerance
Pharmacokinetic tolerance is when the body gets better at removing the drug. (e.g. from barbituates)
Cellular tolerance is when the cells become less responsive to the drug. (e.g. from alcohol)
Pharmacokinetic Tolerance:
What happens: Your body gets better at processing the drug over time.
How: Your liver or kidneys may become more efficient at breaking down or eliminating the drug, so it doesn’t have the same effect.
Example: If you take a drug regularly, your liver might start clearing it faster, so you need more of the drug to feel the same effect.
Cellular Tolerance:
What happens: Your cells become less responsive to the drug over time.
How: The receptors in your cells that the drug affects might become less sensitive or fewer in number, so the same amount of the drug has less impact.
Example: If you use a drug like painkillers often, the cells in your nervous system might start reacting less to the drug, so it doesn’t relieve pain as well as it used to.
Cytochrome p450 metabolises other drugs such as warfarin, digoxin, oral contraceptive, TCAs. Therefore, what will happen to the clinical efficacy of these drugs if the subject taking them is dependent on barbituates
barbituate tolerance (type of pharmacokinetic tolerance)= is due to drug-evoked induction of cytochrome P450 enzymes in liver= results in faster metabolism of barbiturates
so in patients with barbituate tolerance the clinical efficacy of the listed drugs would be reduced
what is meant by:
- zero order kinetics
- first order kinetic
Zero order kinetics= a drug concentration independent elimination rate process i.e. drug is eliminated at a constant rate (n.b. alcohol metabolism is zero order kinetics)
First order kinetics= a drug concentration dependent elimination rate process i.e. more drug is present, the more drug will be eliminated
the dependence producing properties of opiates are due to stimulation of mu-type opioid receptors. Opiates stimulate mu-receptors and cause hyperpolarisation by increasing K+ conductance. The net effect leads to inhibit nerve cell firing and inhibit transmitter release.
Explain the 3 types of opioid receptors + what each is responsible for
mu= responsible for euphoria, analgesia, respiratory depression and constipation caused by opiates
kappa= role in analgesia at spinal level and cause sedation but does NOT contribute to dependence on opiates
delta= analgesia
Which receptors are the cellular target of the compound delta-9- tetrahydrocannabinol?
Delta-9-tetrahydrocannabinol (Δ⁹-THC) primarily targets CB1 and CB2 receptors.
CB1 receptors are mainly found in the central nervous system (CNS) and mediate psychoactive effects.
CB2 receptors are mostly in the immune system, influencing inflammation.
Both CB1 and CB2 receptors belong to the G-protein-coupled receptor (GPCR) family.
What is ‘ecstasy’? Name two neurotransmitter systems involved in the effects of this compound.
Ecstasy (MDMA) is a psychoactive drug known for its stimulant and hallucinogenic effects. It enhances mood, energy, and social bonding by increasing neurotransmitter activity.
Two neurotransmitter systems involved:
Serotonin (5-HT) System – MDMA increases serotonin release, leading to mood elevation, emotional warmth, and altered perception.
- Dopamine System – It also boosts dopamine levels, contributing to increased energy and feelings of pleasure.
How do the benzodiazepines exert their effects on the central nervous system?
Benzodiazepines enhance the effect of the neurotransmitter gamma-aminobutyric acid (GABA) at the BZD site on the GABA_A receptor, leading to increased neuronal inhibition and central nervous system depression.
what are barbiturates; common effects
Barbiturates are central nervous system depressants that enhance GABAergic inhibition.
produce sedative, hypnotic, and anticonvulsant effects.
examples: phenobarbital, hexobarbital.
What is methadone?
Methadone is a synthetic opioid medication primarily used for pain management and the treatment of opioid use disorder (OUD).
Methadone functions as a full agonist at the μ-opioid receptor, effectively mimicking the pain-relieving properties of endogenous opioids. It also acts as an antagonist at (NMDA) receptors and inhibits the reuptake of serotonin and norepinephrine, contributing to its analgesic effect
What is the effect of alcohol on voltage-gated calcium channels?
Alcohol inhibits voltage-gated calcium channels (VGCCs), reducing calcium ion influx into neurons. This dampens synaptic transmission, impairing neurotransmitter release, and contributing to alcohol’s sedative effects, cognitive impairment, and motor coordination issues.
Alcohol dampens the neurotransmitter glutamate (excitatory) by inhibiting NMDA receptors, and enhances GABA (inhibitory) activity by increasing its effects on GABA_A receptors. This leads to sedation, impaired cognition, and reduced anxiety.
What is the effect of caffeine on the enzyme phosphodiesterase?
Caffeine inhibits the enzyme phosphodiesterase (PDE).
Phosphodiesterase is responsible for breaking down cyclic AMP (cAMP), a molecule involved in many cellular signaling processes. By inhibiting PDE, caffeine increases the levels of cAMP in cells.
This leads to enhanced cellular responses, such as increased heart rate, vasodilation, and improved alertness, which are characteristic effects of caffeine.
what is the difference between echoic memory and iconic memory
echoic memory= short-lived persistence of auditory sensory memory trace
iconic memory= short-lived persistence of the visual sensory memory trace
narrowing of the cerebral aqueduct leads to what pathology?
Narrowing of the cerebral aqueduct leads to hydrocephalus. Common symptoms of hydrocephalus are bilateral vertical gaze palsy, headaches, nausea, difficulty focusing the eyes, and unsteady gait
periaqueductal grey modulates what kind of info?
The periaqueductal grey modulates pain information coming into the central nervous system.
lesions to what areas of the brain will result in deficits in visuospatial working memory (If the lights suddenly go out and you are left in darkness, visuospatial working memory is what allows you to remember where things are that you can no longer see)
PATIENTS WITH OCCIPITO-PARIETAL LESIONS have problems with visuospatial working memory, particularly:
- inferior posterior parietal lobe; Supramarginal gyrus (Broadmann area 40)
- anterior occipital cortex/ extrastriate cortex (Broadmann area 19)
as the connection between the occipito-parietal region is important for visuo + spatial memory
when doing an active task which requires a higher memory load, what area of the brain is activated
dorsolateral prefrontal cortex (DLPFC) = key to functioning of working memory
+ as time went on the activation of Broca’s (BA44) was transient + more prolonged as memory load increased
What is refractory epilepsy vs intractable epilepsy
Refractory epilepsy (Aka drug resistant epilepsy) occurs when your antiepilepsy medicines are no longer controlling your seizures. Often the cause of refractory epilepsy is not known
Intractable epilepsy is when seizures can’t be completely controlled by medicines. (Intractable means “not easily managed or relieved.
what is anterograde amnesia vs retrograde amnesia
anterograde amnesia= loss of memory for events + knowledge that occur after brain damage
(normal short term memory, normal working memory, normal procedural memory) n.b. they just don’t remember the episodes during which they learned or observed the info previously
retrograde amnesia= loss of memory for events + knowledge that occured before brain damage
What is the first step in memory formation?
Sensory input is processed in the cortical association areas and perirhinal/parahippocampal cortices.
What is the role of the entorhinal cortex in memory?
It acts as a gateway, transferring processed sensory information to the hippocampus.
What function does the dentate gyrus perform in memory?
It separates similar memories to prevent confusion (pattern separation)
How does the hippocampus process and encode new memories?
Through the dentate gyrus, CA3 (pattern completion), CA1, and subiculum before sending processed memory back to the cortex.
Where are long-term memories stored?
Initially in the hippocampus but later consolidated in the cortical association areas.
what is the role of the fornix in memory formation
Connects: Hippocampus to memory regions (mammillary bodies, thalamus).
Supports: Encoding, consolidation, and retrieval of memories.
Key Memory Types: Spatial and episodic memory.
Damage Effects: Causes memory deficits (e.g., anterograde amnesia).
Disease Role: Early involvement in Alzheimer’s disease.
Research Insight: Fornix integrity (via Diffusion tensor imaging; DTI) correlates with memory performance.
Function: Primary output pathway of the hippocampus.
Circuit: Part of the Papez circuit (emotional processing and memory).
Therapeutic Potential: Fornix stimulation studied for memory disorder treatments.
What Happens if the Fornix is Damaged? (clinical relevance)
- Fornix lesions (due to stroke, tumors, or surgery) can cause anterograde amnesia, where patients cannot form new memories.
- Damage to the fornix is also linked to Korsakoff’s syndrome, a condition seen in chronic alcoholics due to thiamine (Vitamin B1) deficiency, which results in severe memory loss.
- Studies using fornix deep brain stimulation (DBS) have explored ways to improve memory in Alzheimer’s disease patients.
Is the Papez circuit the limbic system?
No, the Papez circuit is part of the limbic system. It is a specific pathway for emotion and memory, while the limbic system is a broader network including the amygdala, hypothalamus, and more.
What is the cellular mechanism of Long- term potentiation (LTP)
- Glutamate binds AMPA receptors, depolarizing the neuron.
- Depolarization removes Mg²⁺ block from NMDA receptors.
- Ca²⁺ influx through NMDA receptors activates CaMKII and PKC.
- AMPA receptors are phosphorylated and inserted into the membrane.
- Structural and genetic changes strengthen the synapse long-term.
What’s the difference between NMDA and AMPA receptors?
NMDA: Requires glutamate + depolarization, allows Ca²⁺ influx, slow kinetics, critical for LTP.
AMPA: Activated by glutamate alone, fast kinetics, mediates fast synaptic transmission.
Define Multiple Sclerosis
Pathological Definition: Inflammatory disease of the CNS characterised by demyelination and variable degrees of axonal loss and gliosis.
Clinical Definition: Objective CNS dysfunction, i.e. involvement of two or more white matter structures separated by time (1 month), with no other aetiology.
what is the gross pathology + histopathology of Multiple Sclerosis
Gross Pathology: Lesions/plaques in periventricular white matter, optic nerves, brainstem, cerebellum, and spinal cord. Fresh lesions: pink/gray; older lesions: yellow/tan.
Histopathology:
Perivascular inflammation (T-cells, B-cells, macrophages).
Demyelination (visible with myelin stains).
Axonal loss and gliosis (astrocytic scarring).
Active Lesions: Ongoing demyelination, inflammation, myelin-laden macrophages.
Chronic Lesions: Astrocytic scarring, reduced inflammation, axonal loss, possible remyelination (shadow plaques).
How is Multiple Sclerosis diagnosed?
Clinical - typical clinical course (relapse-onset (CIS/RR/SPMS) or PPMS ) / exclusion of other diseases
MRI - abnormal white matter
Evoked Potentials - delayed conduction
CSF - immunological abnormalities; intrathecal oligoclonal IgG bands (OCBs)
Clinical symptoms + signs of multiple sclerosis
Clinical (Symptoms and Signs – positive and negative phenomena);
Motor - spasticity, weakness, gait abnormalities, spasms (clonic, tonic and flexor)
Sensory - positive (pins & needles, pain, etc.) and negative sensory phenomena (loss of sensation).
Cerebellum - incoordination, ataxia, nystagmus, dysarthria, etc.
Brain Stem - diplopia, vertigo, nystagmus, dysarthria
Optic Nerves - optic neuritis (blurred vision)
Bladder and Bowel – incontinence, frequency, urgency, hesitancy
Higher Functions – cognitive impairment, rarely dementia, depression, poor concentration
Fatigue – complex (exercise-induced, temperature-related)
what do 75% of individuals with multiple sclerosis die from
75% of people with MS die of MS-related complications (aspiration pneumonia or septicaemia from UTIs)
Treatment for Multiple Sclerosis
Disease Modifying;
Acute Relapse – high-dose corticosteroids
Relapsing cases - interferon beta, glatiramer acetate, teriflunomide, fumarates (dimethyl fumarate, diroximil fumarate), S1P modulators (fingolimod, siponimod, ozanimod, ponesimod), natalizumab (anti-VLA4), alemtuzumab (anti-CD52), mitoxantrone, cladribine, anti-CD20 (ocrelizumab, ofatumumab, ublituximab), AHSCT
Progressive MS - ocrelizumab for PPMS and siponimod for active-SPMS (relapse and/or MRI activity) / unmet need for neuroprotection and other add-on treatments.
Symptomatic;
E.g. Spasticity (baclofen, tizanidine, gabapentin, diazepam)
if someone has gait ataxia; reduced voluntary control of movement it indicates dysfunction in the cerebellum (efferent) and/or sensory systems (afferent)
What do absent vs retained reflexes indicate
Absent reflexes= peripheral neuropathy, ganglionopathy or radiculopathy
Retained reflexes= spinal cord disease
What conditions cause cerebellar dysfunction?
Acquired: Stroke, trauma, infections, toxins, tumors, autoimmune disorders (multiple sclerosis, paraneoplastic syndromes, gluten ataxia)
Hereditary: Spinocerebellar ataxias, Friedreich’s ataxia, ataxia-telangiectasia, Wilson’s disease (copper accumulation)
Developmental: Cerebellar hypoplasia, Dandy-Walker malformation (a congenital condition where the cerebellum does not develop normally).
Degenerative: Cerebellar degeneration, multiple system atrophy.
Metabolic: Vitamin deficiencies (B1,B12,E), hypothyroidism.
What is Joubert syndrome?
Joubert syndrome is a rare genetic condition characterized by abnormal brain development that includes the absence or underdevelopment of the cerebellar vermis (an area of the brain that controls balance and coordination) and a malformed brain stem
Joubert Syndrome is a group of recessive disorders characterized by cerebellar hypoplasia, cognitive impairment, low muscle tone, and eye movement abnormalities. It is associated with poor survival rates, with only about 50% of affected individuals living past 5 years of age
what is Friedreich’s ataxia and what is it caused by?
Friedreich’s ataxia is a rare, autosomal recessive neurodegenerative disorder that damages the spinal cord, peripheral nerves and the cerebellum
Friedreich’s ataxia is caused by a defect (mutation) in a gene labeled FXN, which carries the genetic code for the production of a protein called frataxin
A 29 yr old male with early multiple sclerosis complains of difficulty playing squash; 15 minutes in he keeps missing the ball, why is this?
Heat Sensitivity (Uhthoff’s Phenomenon); because body temp goes up; which can temporarily worsen MS symptoms (e.g., coordination, vision, or muscle control)
MS-related fatigue is a common symptom that worsens with physical exertion.
What nucleus in the hypothalamus controls the 24 hour circadian rhythm?
The suprachiasmatic nucleus (SCN) in the hypothalamus controls the 24 hour circadian rhythm.
Neurons of the SCN increase their activity during the day/light phase and decrease their activity during the dark phase
a loss of which type of neuron in the hypothalamus causes narcolepsy?
A loss of orexin neurons/ orexin deficiency= narcolepsy (condition characterised by excessive sleepiness; increased frequency of falling asleep in the daytime)
Why does half-life matter when it comes to benzodiazepines? Give examples of short half-life benzodiazepines
Short-acting benzodiazepines have a shorter half-life. This means that the drugs are processed and leave your body more quickly. Short-acting drugs have a higher risk of withdrawal symptoms.
short half-life benzodiazepines: Oxazepam, Temazepam, Triazolam
Non-benzodiazepine hypnotics
Zaleplon, Zolpidem, Zopiclone, Eszopiclone
Selective mutism is usually associated as a result of anxiety, what is it?
A condition where a person (usually a child) consistently fails to speak in specific social situations (e.g., school) despite being able to speak in other settings. It is often linked to anxiety.
where do symptoms of anxiety/fear originate in the brain
The central nucleus of the amygdala (CEA) acts as the primary output hub for the amygdala, sending projections to coordinate the fear response.
These projections include:
- lateral hypothalamus= heart rate, blood pressure
- dorsal vagal N.= bradycardia, ulcers
- parabrachial N.= panting, respiratory distress
- basal forebrain= arousal, vigilance, attention
- reticular pontis caudalis= increased startle response
- central gray area= freezing, social interaction
- paraventricular n.= corticosteroid release
What is the first-line treatment for anxiety disorders according to NICE?
Cognitive Behavioral Therapy (CBT) is the first-line treatment for most anxiety disorders. This includes individual or group CBT sessions and guided self-help materials.
What are the second-line treatments for anxiety disorders according to NICE?
SSRIs (e.g., Sertraline, Escitalopram) are the first-choice medications. If SSRIs are not suitable, SNRIs (e.g., Venlafaxine) or Pregabalin may be used. Benzodiazepines are only for short-term use in crisis situations.
what does Anterior Cerebral Artery (ACA) supply
The Anterior Cerebral Artery (ACA) supplies the frontal, pre-frontal and supplementary motor cortex, as well as parts of the primary motor and primary sensory cortex
Which arteries supply the orbitofrontal cortex (OFC)?
What is the function of the orbitofrontal cortex (OFC)?
The orbitofrontal (or frontobasal) arteries (OFAs) are the medial (MOFA is branch of ACA) and lateral (LOFA) orbitofrontal artery (branch of MCA)
function of the orbitofrontal cortex (OFC):
- regulates our actions in response to reward and punishment
- it controls/regulates our primitive urges for food, sex.
- damaged here leads to behavioural disinhibition i.e. inappropriate social or sexual behaviour
The orbitofrontal cortex is clinically significant because damage of the OFC through acquired brain injury typically leas to a pattern of disinhibited behaviour. Give examples of symptoms in patient with OFC damage
- decreased emotional responses/ poor empathising ability
- swearing excessively
- hypersexuality
- poor social interaction
- compulsive gambling
- drug use
What is conduction aphasia and damage to what brain area results in it
damage to the arcuate fasciculus (connects Wernicke’s + Broca’s) results in conduction aphasia
Conduction aphasia= someone has trouble repeating words or sentences, even though they understand them and can speak fluently
e.g. if someone says “refrigerator,” a person with conduction aphasia might say “refritigator” or struggle to say it correctly at all, even though they know what it means
what happens when you damage the superior longitudinal fasciculus vs inferior longitudinal fasciculus
Superior Longitudinal Fasciculus (SLF);
- Connects frontal lobe to other brain regions.
- Damage → Language issues, attention deficits, motor coordination problems.
Inferior Longitudinal Fasciculus (ILF);
- Connects occipital & temporal lobes (visual processing).
- Damage → Face blindness (prosopagnosia), object recognition issues (visual agnosia).
The visual cortex (V1) projects to the posterior parietal association cortex via the ____ ____ ____
The visual cortex (V1) projects to the inferotemporal association cortex via the ____ ____ ____
The visual cortex (V1) projects to the posterior parietal association cortex via the superior longitudinal fasciculus (this pathway shows us where is the object)
The visual cortex (V1) projects to the inferotemporal association cortex via the inferior longitudinal fasciculus (this pathways shows us what is the object)
what is apperceptive visual agnosia, and lesions to what areas of the brain cause it?
Definition: Inability to perceive and recognize objects due to deficits in early-stage visual processing. Difficulty in copying, matching, or identifying objects, especially from unusual angles or incomplete details. Basic visual functions like brightness and color perception remain intact.
Medically Characterized By:
- Constructional Apraxia: Trouble constructing 3D objects.
- Oculomotor Apraxia: Inability to move eyes toward an object.
- Piecemeal Perception: Only perceiving small local aspects of stimuli.
Lesions:
Lateral Occipital Cortex (LOC) – Important for shape/object perception.
Dorsal Stream (Occipito-parietal pathway) – Involved in spatial processing.
Ventral Stream Disruptions (Occipito-temporal pathway) – Affecting object recognition.
Causes:
Stroke
Carbon monoxide poisoning
Traumatic brain injury (TBI)
Degenerative conditions (e.g., Alzheimer’s disease)
What deficits would you see if the Superior Longitudinal fasciculus (SLF) was damaged?
Conduction aphasia= as arcuate fasciculus is part of SLF; this type of aphasia is characterised by fluent speech with frequent errors + difficulty repeating words
Spatial Neglect – Difficulty perceiving or attending to one side of space (often seen in right hemisphere damage).
Poor Spatial Awareness – Trouble estimating distances or recognizing spatial relationships.
Impaired Motor Coordination – Difficulty with hand-eye coordination and movement planning.
N.b. SLF is responsible for “WHERE? do u see it” its the dorsal pathway which tells us spatial info, language processing + motor coordination
What deficits would you see if the Inferior Longitudinal fasciculus (ILF) was damaged?
Associative Visual Agnosia: Difficulty recognizing objects despite intact vision.
Prosopagnosia: Impaired ability to recognize familiar faces.
Visual Amnesia: Challenges in recalling visual information
N.B. the ILF is responsible for “WHAT? do you see” it is crucial for object + face recognition, as well as visual memory
Hemispatial neglect is usually tested for by asking the patient to draw a clock. What is it, and lesions to what brain areas cause it
Hemispatial Neglect is a neuropsychological condition where a person fails to attend to or recognize stimuli on one side of their visual field, typically the left side, despite having normal sensory function.
- the patient is unaware of the deficit (unlike in hemianopia where they are aware)
lesions associated with neglect:
- right posterior parietal cortex
- inferior parietal lobe
- temporoparietal junction (TPJ)
n.b. these are usually stroke victims but can be seen in Alzheimer’s
What is Balint’s syndrome?
Balint’s syndrome is caused by a bilateral parieto-occipital lesion
characterised by:
Simultanagnosia= inability to identify multiple objects simultaneously + conceptualise the whole picture despite the ability to identify individual items in the same screen (e.g. a forest picture can identify individual trees but not the forest)
Optic ataxia= impairment of visual control leading to misdirection of the arm to the visual object of interest associated with defective hand orientation + grip formation
Oculomotor apraxia= inability to move eyes towards an object (despite intact extra-ocular muscle function)
What is acquired prosopagnosia and lesions to which brain area cause it?
Acquired prosopagnosia= person cannot recognise faces despite having normal vision + cognitive function
Lesion: fusiform gyrus (section of infero-temporal cortex)
what is consciousness, wakefulness and awareness
consciousness= state of full awareness of self + environment
wakefulness= ability to have basic reflexes such as open eyes, cough, swallow, suck
awareness= ability to carry out complex thought processes
What nucleus of the hypothalamus promotes arousal vs sleep
The tuberomamillary nucleus (TMN)= promotes arousal
whereas
The ventrolateral preoptic nucleus (VLPO)= promotes sleep
difference between stupor and coma
Stupor: A state of deep unresponsiveness where a person is only partially conscious and can be briefly awakened with strong stimuli (e.g., pain or loud noise), but quickly returns to an unresponsive state.
Coma: A complete loss of consciousness where the person cannot be awakened by any stimuli and shows no purposeful responses.
What is locked-in syndrome and usually its a result of injury to which part of the pons?
Locked-in syndrome is usually a result of damage to the VENTRAL pons (causing interruption to corticospinal + corticobulbar tracts) this caues quadriplegia + anarathria (mute)
Locked-in syndrome is a state of unresponsiveness in which patient lies with eyes closed + cannot be aroused to respond appropriately to any stimuli. However, patient retains eye movement + are fully conscious
often misdiagnosed as coma/vegtative state
communications via e-Tran Fram or brain computer interface
what is the pineal gland, its function + location
the pineal gland, which is a small pea-shaped endocrine gland and is responsible for the production of melatonin.
It is found posterior to the hypothalamus, and in between the left and right cerebral hemispheres.
Sumatriptan mechanism of action
Sumatriptan is a 5-HT1B/D agonist
is a drug used to treat migraines and cluster headaches. It belongs to the ‘triptan’ family of drugs, which work by binding to and activating 5-HT1B and 5-HT1D receptors. Through its 5-HT1B/D agonist activity, CGRP (calcitonin gene-related peptide) release is inhibited, which is responsible for the drug’s therapeutic effect. Activation of these receptors also results in vasoconstriction of cerebral vessels, which is involved in migraine relief.
Severe cases of Guillain-Barre syndrome can cause locked-in syndrome. What is Guillain-Barre syndrome
Guillain-Barre syndrome is an autoimmune disorder in which the immune system attacks healthy neurones
The main symptoms are weakness or paralysis of the muscles that move the eyes, problems with balance and coordination, and abnormal or no reflexes. People with this disorder may have other common GBS symptoms like muscle weakness
Most people recover completely from Guillain-Barre syndrome, but some serious illnesses can be fatal. While recovery may take up to several years, most people are able to walk again six months after symptoms first began.
What is Minimally conscious state (MCS)?
Minimally conscious state (MCS)= condition of severely altered consciousness, behavioural evidence of self or environmental awareness
- recognise verbal or gestural yes or no responses
- provide simple verbal
- follow simple commands
- provide purposeful movements (e.g. smile, raise a limb, use objects (hairbrush) in a consistent manner)
- often after passing through coma + vegetative state
What is the difference between confusional and post-confusional state
Confusional state:
- interactive communication
- amnesia/confusion (weeks-months)
- hypokinetic or agitated
- labile behaviour (e.g. rapid + exagerated mood changes- laughing/crying)
Post-confusional state:
- resolution in amnesia/confusion (months-years)
- cognitive impariments in higher levels; attention, memory retrieval, + executive functioning
- deficits in self-awareness, social awareness, behavioural + emotional regulation
- achieve functional independence in daily self-care
When patients are in comatose, vegetative or minimally conscious state what medication is used for the following:
- opioid for moderate-severe pain
- sedation
- reduce saliva production in airway
Oxycodone- opioid for moderate-severe pain
Midazolam- sedation
Glycopyrronium- reduce saliva production in airway
Which cranial nerves are responsible for the gag reflex and soft palate elevation?
✅ Gag Reflex (Pharyngeal Reflex):
Afferent limb (sensory): Glossopharyngeal nerve (CN IX)
Efferent limb (motor): Vagus nerve (CN X)
✅ Soft Palate Elevation:
Muscle involved: Levator veli palatini
Innervation: Vagus nerve (CN X) via the pharyngeal plexus
💡 Function: Prevents choking & ensures proper swallowing!
activation of which receptor leads to dysphoria?
kappa opioid receptor activation leads to dysphoria (emotional distress)
Explain the role of dynorphin + the mechanism which underlies the development of withdrawal
- reward is associated with release of dopamine
- drugs of abuse can ultimately lead to up-regulation of the opioid peptide dynorphin
- activation of kappa opioid receptors by dynorphin can trigger dysphoria, by reducing dopamine release; withdrawal is associated with dysphoria
What drug is recommended for the treatment of treatment resistant schizophrenia
Clozapine; 5-HT2 + DA receptor agonist
reduces symptoms of schizophrenia + limits substance misuse
Schizophrenia is associated with decreased glutamatergic transmission. Which ligand is a co-agonist of glutamate at the NMDA receptor?
glycine is a co-agonist of glutamate at the NMDA receptor
which type of memory is needed to require facts learnt at school
semantic memory= (subcategory of declarative memory) a type of long-term memory involving the capacity to recall words, concepts, or numbers, which is essential for the use and understanding of language.
what type of memory is needed to remember your personal history
autobiographical memory
what is declarative memory
a type of long-term memory that involves conscious recollection of particular facts and events.
There are 2 types:
- Episodic Memory: Deals with personal experiences and specific events in time (e.g., remembering your last birthday party).
- Semantic Memory: Refers to general knowledge and facts about the world, independent of personal experience (e.g., knowing that Paris is the capital of France).
Which type of memory is needed to remember how to do things?
procedural memory
