Brain + Behaviour wk1+2 Flashcards

Question

what is the role of serotonin in the nervous system

Answer 1

Serotonin= Involved in mood and sensory perception regulation, pain modulation, bowel function, and appetite (the gut provides around 95% of total body serotonin).

Answer 2

Pabrinex (replaces vitamin B1/thiamine ,B2,B3, B6, C glucose for energy metabolism) is indicated for rapid treatment of severe depletion or malabsorption of vitamins B and C, particularly in alcoholism, after acute infection occurring post-operatively or in psychiatric settings

Answer 3

the resting potential of a central neurone is due to : K+ leaking out through non gated K+ channels

Answer 4

Association motor areas include a large variety of brain regions (prefrontal, parietal, temporal, and occipital cortices) where, for some, not only different sensory modalities combine and motor planning occurs, but attention is shifted and memories are stored.

Answer 5

A cortical area of the LEFT hemisphere specialised in the production of speech movements Broca's area is no longer activated by the time speech commences, showing that its role is one of planning rather than producing speech Broca’s area coordinates the linkage between: the articulatory representations (motor cortex) and the sensory representation of words (temporal cortex)

Answer 6

damage to Broca's area= motor/expressive aphasia a nonfluent aphasia that makes it difficult to write or speak thoughts, even when the speaker knows what they want to say Speak in short (< 4 words) or incomplete sentences Substitute one word for another or one sound for another Speak in sentences that don't make sense Difficulty writing Retain the ability to read and understand speech i.e. comprehension preserved, but expression impaired

Answer 7

the frontal eye fields are in Brodmann area 8 the FEF are anterior to the motor strip in the frontal lobes= brodmann area 8 this area receives input from the occipital lobes and sends output to the extraocular muscles through the pontine nuclei, reticular formation, superior coliculus, basal ganglia + cerebellum

Answer 8

the FEF are important for initiation of SACCADES + SMOOTH PURSUIT; used to locate objects for survival Saccades: - small, rapid jerky movements of the eyes - Speed: Very fast (up to 900°/s) - Function: Used to quickly reposition the fovea (the central part of the retina responsible for sharp vision) onto objects of interest. e.g. reading, scanning a crowd, looking at objects in quick succession Smooth pursuit: - Slow, continuous eye movements used to track a moving object -Speed: Much slower than saccades (typically 30–100°/s) - Function: Keeps a moving object in focus on the fovea, allowing for clear vision while tracking. e.g. Watching a moving car, tracking a flying bird, following a finger n.b. smooth pursuit requires a moving target; cannot be performed voluntarily without a stimulus.

Answer 9

Apraxia: the loss of ability to execute or carry out skilled movement and gestures despite having the physical ability and desire to perform them (“praxis” = skilled action)

Answer 10

Bilateral damage to the FEFs produces oculomotor apraxia Patients cannot move their eyes horizontally and move them quick enough to follow a moving object or read a line of text They automatically turn their head in order to compensate for the lack of eye movement They often move their head too far and have to move several times to get the desired object on their fovea

Answer 11

FEFs lesion; eyes drift ipsilaterally (towards the lesion side) Pons lesion= eyes drift contralaterally (away from the lesion side)

Answer 12

The sensory representation of words happens in the temporal cortex In the temporal cortex acoustic and visual representations of words are stored

Answer 13

Aphasia is a language disorder caused by damage to the brain, typically in areas responsible for language processing, such as Broca’s area or Wernicke’s area (usually in the left hemisphere). It affects a person’s ability to speak, understand, read, or write but does not impact intelligence. An aphasic patient (someone who suffers from aphasia)

Answer 14

pyramidal tract decussates at the spinomedullary junction (spinal cord+medulla junction) injury above deccusation= effect seen on contralateral (opposite) side injury below deccusation= effect seen on ipsilateral side

Answer 15

In the ventral horn, the α motor neurons supplying distal extensor muscles are located LATERALLY and VENTRALLY In the ventral horn, the α motor neurons supplying proximal flexor muscles are located MEDIALLY and DORSALLY

Answer 16

the 'small' anterior/ ventral corticospinal tract terminates at mid-thoracic level

Answer 17

In the spinal level it innervates

Answer 18

Controls voluntary movements of the head and neck Corticobulbar tract supplies upper motor neuron innervation to the cranial nerves supplying head and face. Corticobulbar tract carries upper motor neuron input to motor nuclei of trigeminal, facial, glossopharyngeal, vagus, accessory, and hypoglossal nerves

Answer 19

1. Spasticity Definition: Spasticity is a condition where muscles are stiff, tight, and resistant to movement due to increased muscle tone (hypertonia). Cause: It results from damage to the upper motor neurons (UMNs) in the brain or spinal cord, leading to disrupted inhibitory control over reflexes. 2. Clonus Definition: Clonus is a rhythmic, involuntary muscle contraction and relaxation (jerky movements) in response to a sudden stretch. Cause: It occurs due to hyperactive stretch reflexes caused by upper motor neuron lesions. 3. Hyperreflexia Definition: Hyperreflexia is an exaggerated reflex response due to loss of normal inhibitory control from the brain. Cause: It results from upper motor neuron damage, leading to overactive reflex loops in the spinal cord.

Answer 20

When CST is damaged the extrapyramidal system becomes hyperactive = resulting in hyperactive stretch reflexes + spasticity

Answer 21

Decerebrate posture: A rigid extension of the arms and legs, with wrists rotated outward (pronated), legs straight, and toes pointed downward (plantar flexion). Cause: Damage to the brainstem (below the level of the red nucleus), affecting the midbrain or pons. This disrupts inhibitory control from the cortex, leading to excessive extensor muscle activity. Decorticate Posture: Abnormal flexion of the arms towards the core ("mummy pose"), with legs extended and toes pointed downward. Cause: Damage to the corticospinal tract above the brainstem, typically at the level of the cerebral hemispheres, internal capsule, or thalamus. This disrupts motor control but spares brainstem reflexes.

Answer 22

paresis= a condition in which muscle movement has become weakened or impaired. paraesthesia= an abnormal sensation, typically tingling or pricking (‘pins and needles’), caused chiefly by pressure on or damage to peripheral nerves.

Answer 23

Pyramidal tracts: 1. Corticospinal Tract * Origin: Arises from the primary motor cortex (Brodmann area 4), premotor cortex (area 6), and parts of the somatosensory cortex. - Decussation: LATERAL CORTICOSPINAL TRACT (85-90% of CST fibres) cross at the pyramidal decussation in the lower medulla ANTERIOR CORTICOSPINAL TRACT remaining fibers continue ipsilaterally decussate in the spinal cord - Spinal Cord Pathway: - Lateral Corticospinal Tract: Descends in the lateral funiculus, terminating at various spinal levels to control distal limb muscles. - Anterior Corticospinal Tract: Travels in the anterior funiculus, primarily influencing axial and proximal limb muscles. anterior CST function: Gross motor and postural control lateral CST function: Fine motor and precise voluntary movement 2. Corticobulbar Tract * Origin: Similar to the corticospinal tract, it originates from the motor cortex. * Decussation: Fibers innervate cranial nerve nuclei bilaterally, except for parts of the facial nerve (CN VII) and hypoglossal nerve (CN XII), which receive predominantly contralateral input. * Pathway: Descends through the genu of the internal capsule to the brainstem, terminating in motor nuclei of cranial nerves. * Role: Controls muscles of the face, head, and neck, facilitating functions like facial expression, mastication, and swallowing.

Answer 24

Extrapyramidal Tracts These tracts originate from subcortical structures and modulate involuntary motor activities, posture, and muscle tone. 1. Rubrospinal Tract * Origin: Red nucleus in the midbrain. * Decussation: Fibers cross immediately in the midbrain. * Spinal Cord Pathway: Descends in the lateral funiculus, anterior to the lateral corticospinal tract. FUNCTIONS: modulation of motor tone (flexors contract, extensors relax + vice versa), modulation of reflex activity (red nucleus is connected with reticular formation) 2. Reticulospinal Tract * Origin: Reticular formation in the pons and medulla. * Decussation: Predominantly uncrossed * Spinal Cord Pathway: Divided into medial (pontine) and lateral (medullary) tracts, descending in the anterior and lateral funiculi, respectively. FUNCTIONS: Controls the activity of lower motor neurons (general excitability of spinal cord), posture maintenance, control of autonomic functions (heart rate, circulation, respiratory rate) 3i. The lateral Vestibulospinal Tract * Origin: Vestibular nuclei in the upper medulla/ lower pons Spinal cord pathway: projects ipsilaterally in the anterior quadrant to antigravity muscles of lower body + legs FUNCTIONS: upright posture maintenance (controls posture and balance) 3ii. The medial Vestibulospinal tract Origin: a continuation of the medial longitudinal fasciculus (occulomotor reflex, saccadic eye movements, vestibular-ocular reflex, smooth pursuit) FUNCTIONS: head + eye coordination, maintains upright posture of head + neck 4. Tectospinal Tract * Origin: Superior colliculus in the midbrain. * Decussation: Fibers cross in the midbrain. * Spinal Cord Pathway: Descends in the anterior funiculus, terminating primarily in cervical segments. * Role: Mediates head and neck movements in response to visual and auditory stimuli.

Answer 25

the arcuate fasciculus (AF; from Latin 'curved bundle') is a bundle of axons that generally connects Broca's area and Wernicke's area in the brain. It is an association fiber tract connecting caudal temporal lobe and inferior frontal lobe

Answer 26

pre-frontal syndrome= following the lesion, behaviour becomes automatic habitual, stimulus-driven; loss of 'goal-orientated behaviour' - dramatic behavioural + personality changes

Answer 27

OFC function: values + expected values based on knowledge and experience e.g. - Decision-Making & Value-Based Choices - Emotion & Social Behavior Regulation - Reward & Punishment Processing - Impulse Control & Behavioural Flexibility Damage to the OFC can lead to: Orbitofrontal syndrome: ❌ Impulsivity & Poor Decision-Making (e.g., reckless financial choices) ❌ Lack of persistence/planning ❌ Lack/blunted emotional Regulation/experience (e.g., inappropriate anger or laughter) ❌ Socially Inappropriate Behavior (e.g., rudeness, lack of empathy) ❌ Difficulty Learning from Consequences (e.g., continuing risky behaviour despite negative outcomes)

Answer 28

function of the medial prefrontal cortex (mPFC): - directs the correct emotional or motor response in light of the knowledge acquired from past experience - regulates fight or flight by working w amygdala damage to mPFC: - Social withdrawal, inappropriate behavior - Risky behavior, stubbornness - apathy, loss of interest in goals - Poor self-reflection, lack of insight dorso-ventral gradient (dmPFC, rmPFC, vmPFC); as we go more: - dorsal= controls of actions - ventral= emotional/autonomic responses

Answer 29

fight-or-flight response is controlled by the limbic system (amygdala, hippocampus, parahippocampal gyrus, cingulate cortex, septal nuclei, mamillary body, fornix, hypothalamus) particularly the amygdala, which activates the hypothalamus to trigger the body's stress response

Answer 30

dorsolateral prefrontal cortex = Brodmann 9 + 46 frontal pole = 10 after lesion to dorsolateral prefrontal cortex + frontal pole= - lack of ability to plan - apathetic - lack of ability to sequence actions or tasks - poor working memory for spatial info ( RIGHT lesion) - poor working memory for verbal info (if LEFT lesion) - personality changes

Answer 31

The supplementary motor area (SMA)= organises actions based on internal goals + personal experience SMA makes an actual plan for purposeful actions (piano playing) SMA has strong reciprocal connections with medial frontal cortex

Answer 32

the premotor cortex= organises EXTERNALLY sensory-guided actions; selects movement based on external info from primary sensory cortices - has strong reciprocal connections w parietal lobe

Answer 33

the primary motor cortex (M1) is Brodmann area 4; and it's function is the execution of movements M1 receives input from almost all cortical areas involved in motor control lesion of the primary motor cortex results in profound paralysis

Answer 34

The central sulcus separates the frontal and parietal lobes

Answer 35

occipital lobe

Answer 36

Falx cerebri is defined as a sickle-shaped vertical fold of dura mater that separates the two cerebral hemispheres and helps in preventing certain types of brain herniation.

Answer 37

The corpus callosum is the largest white matter structure in the brain Corpus callosum connects the right and left hemispheres of brain; ensures both sides of the brain can communicate and send signals to each other

Answer 38

The Bereitschaftspotential (BP), or "readiness potential," is a slow, gradual electrical signal that appears in the brain before a voluntary movement is performed. N.B. - early component (BP1) is generated by the pre-SMA/SMA + premotor cortex - late component (BP2) is when the neural signal leaves the primary motor cortex The primary sources of BP are: - Supplementary Motor Area (SMA) → Prepares and plans complex, self-initiated movements. - Premotor Cortex (PMC) → Helps with motor planning. - Primary Motor Cortex (M1) → Executes the actual movement. Basal Ganglia & Thalamus → Modulate movement initiation. The BP is strongest over the contralateral motor cortex, meaning if you're moving your right hand, the left hemisphere of your brain shows the most BP activity.

Answer 39

Visual acuity (VA) refers to the sharpness or clarity of vision, specifically how well you can distinguish fine details at a given distance. Snellen's test; patient stands at 20ft or 6 meters away and reads letters i.e. its called 20/20 vision if its perfect because u can see at 20ft

Answer 40

Ishihara plates test for colour blindness

Answer 41

afferent (sensory) limb [CN II]: 1. Retina → Detects light 2. Optic nerve (CN II) → Carries sensory signal 3. Pretectal nucleus (midbrain) → Relays signal to both sides 4. Edinger-Westphal nucleus (EWN, midbrain) → Sends motor output efferent (motor) limb [CN III]: 1. Edinger-Westphal nucleus (midbrain) → Sends motor signal 2. Oculomotor nerve (CN III) → Carries motor signal 3. Ciliary ganglion (parasympathetic ganglion near the eye) → Relays motor signal 4. Sphincter pupillae muscle (iris) → Constricts the pupil

Answer 42

Marcus Gunn pupil aka relative afferent pupillary defect; is when light is shone in the affected eye and both pupils constrict less (or they dilate (compared to when light is shone in unaffected eye)

Answer 43

Conductive Hearing Loss (CHL) → Problem in sound conduction through the outer or middle ear. CHL sound perception: Reduced loudness, but clarity remains CHL causes: Earwax, ear infections, otosclerosis (a form of abnormal bone growth within the middle ear that causes progressive hearing loss) CHL= hearing aids effecitve Rinne test in CHL= negative Weber test in CHL= sound is louder in affected ear Sensorineural Hearing Loss (SNHL) → Problem in the inner ear (cochlea) or auditory nerve (CN VIII). SNHL sound perception: Both loudness and clarity are affected SNHL causes: Aging, noise exposure, nerve damage, ototoxic drugs (e.g. aminoglycoside antibiotics, macrolide antibiotics, loop diuretics) SNHL= hearing aids less effective; COCHLEAR IMPLANTS needed in severe cases Rinne test in SNHL= positive/normal Weber test in SNHL= sound is louder in unaffected ear

Answer 44

Tuning Fork Used for both: 512 Hz tuning fork (best for human speech range) Rinne's test = air + bone conduction Normal hearing or SNHL: Air conduction (AC) > Bone conduction (BC) (Rinne positive). Conductive hearing loss: Bone conduction (BC) > Air conduction (AC) (Rinne negative). Weber's test= differentiates between conductive and sensorineural hearing loss It involves placing a vibrating tuning fork in the middle of the forehead - in normal hearing/symmetrical hearing loss the sound is perceived equally in both ears - in conductive hearing loss, sound is louder in affected ear - in sensorineural hearing loss, sound is louder in unaffected ear

Answer 45

weak cough= problems with closing glottis= vagus nerve lesion

Answer 46

The degeneration of the nigrostriatal pathway and subsequent loss of striatal dopamine contributes to the cardinal clinical motor symptoms: tremor, rigidity, bradykinesia and postural instability

Answer 47

Dopamine receptors are G-protein-coupled receptors excitatory= D1-class receptors (D1 and D5) inhibitory= D2-class receptors (D2, D3, D4)

Answer 48

Blood Supply to the Basal Ganglia: 1. Lenticulostriate Arteries: - Origin: Arise from the M1 (horizontal) segment of the Middle Cerebral Artery (MCA). -Supply: Primarily the putamen, globus pallidus, and parts of the caudate nucleus. - Clinical Note: These arteries are small and lack significant collateral circulation, making them susceptible to occlusion. Blockage can lead to lacunar infarcts, small, deep strokes within the brain. 2. Recurrent Artery of Heubner (Distal Medial Striate Artery): - Origin: Branches from the A1 segment of the Anterior Cerebral Artery (ACA). - Supply: Anterior portions of the caudate nucleus, putamen, globus pallidus, and the anterior limb of the internal capsule. - Clinical Note: Infarction in this artery can affect motor pathways, leading to weakness and other motor deficits. 3. Anterior Choroidal Artery: - Origin: Typically arises from the internal carotid artery. - Supply: Parts of the globus pallidus, tail of the caudate nucleus, and the posterior limb of the internal capsule. - Clinical Note: Occlusion can result in a classic triad of contralateral hemiplegia, hemianaesthesia, and homonymous hemianopia due to its involvement with motor and sensory pathways. Relevance in Stroke: The small size and limited collateral circulation of these arteries make the basal ganglia vulnerable to ischemic strokes. Hypertension is a significant risk factor, as it can lead to the narrowing or occlusion of these vessels. Strokes in the basal ganglia can result in various neurological deficits, including motor impairments, sensory disturbances, and cognitive or emotional changes, depending on the specific nuclei and pathways affected

Answer 49

The parts of striatum are separated by the internal capsule

Answer 50

external capsule

Answer 51

Lentiform nucleus

Answer 52

caudate nucleus

Answer 53

Chorea = (greek; to dance) refers to non-rhythmic, jerky, rapid, nonsuppressible involuntary movement, mostly of the distal muscles + face Athetosis= slow, involuntary, regular writhing movements of the fingers, hands, toes + feet (in some cases arms/legs/neck/tongue) these are movements resulting from lesions to the striatum (often as a result of cerebral palsy Ballismus= a type of chorea, usually involving violent, involuntary flinging of 1 arm/ or 1 leg (usually one side of body affected: 'hemiballismus'). The movements are wider + more intense than chorea. Usually as a result of damage to subthalamic nucleus

Answer 54

Parkinson's disease (PD) is a progressive neurodegenerative disorder primarily affecting motor function. Pathophysiology: PD is characterized by the degeneration of dopaminergic neurons in the substantia nigra pars compacta. This neuronal loss leads to a significant reduction in dopamine levels within the striatum, disrupting the balance of motor control. Pathological Hallmark: The presence of Lewy bodies, which are intracellular aggregates of α-synuclein, is a key pathological feature of PD. Clinical Features: Motor Symptoms: - Bradykinesia: Slowness of movement; a cardinal feature required for diagnosis. - Resting Tremor: Typically a "pill-rolling" tremor observed at rest. - Muscle Rigidity: Increased muscle tone leading to stiffness. - Postural Instability: Impaired balance, often leading to falls. Non-Motor Symptoms: - Autonomic Dysfunction: Orthostatic hypotension, constipation. - Neuropsychiatric Symptoms: - - - Depression, anxiety, cognitive impairment. - Sleep Disturbances: REM sleep behavior disorder, insomnia. Management: Pharmacological Treatment: - Levodopa: Considered the most effective treatment for motor symptoms. It's often combined with a dopa-decarboxylase inhibitor to reduce peripheral conversion. Dopamine Agonists: Such as pramipexole or ropinirole; used in early stages or as adjunct therapy. MAO-B Inhibitors: Like selegiline or rasagiline; can provide mild symptomatic benefit. Non-Pharmacological Treatment: - Physiotherapy: To improve balance and motor function. - Occupational Therapy: Assists with daily living activities. - Speech and Language Therapy: Addresses speech and swallowing difficulties. Advanced Therapies: - Deep Brain Stimulation (DBS): Considered for patients with advanced PD experiencing motor fluctuations not controlled by medication.

Answer 55

parkinsonism; 1) resting tremor 2) rigidity 3) slowness of movement (bradykinesia/akinesia) 4) loss of postural reflexes

Answer 56

- hyposmia (decreased sense of smell) - RBD (rapid eye movement behavioural disorder) - EDS (Excessive Daytime Sleepiness) - Hypotension - Urinary and erectile dysfunction these symptoms are prodromal; appearing years before motor symptoms of Parkinson's manifest

Answer 57

Monitoring of gradual dopaminergic nigral cell loss through dopamine transporter (DaT) imaging in the striatum DaTscan involves an injection of a small amount of a radioactive drug and a machine called a single-photon emission computed tomography (SPECT) scanner, similar to an MRI. The drug binds to dopamine transmitters in the brain, showing where in the brain dopaminergic neurons are.

Answer 58

About 15 percent of people with Parkinson's disease genetic markers; LRRK2, PARK2, PARK7, PINK1 or the SNCA (codes for protein alpha-synuclean) gene

Answer 59

MPTP (1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine) is an organic compound. It is classified as a tetrahydropyridine. MPTP is a precursor to the monoaminergic neurotoxin MPP+, whic is neurotoxic to dopaminergic neurons in the substantia nigra ; hence causes parkinsonism In 1982, seven young adults developed severe and irreversible parkinsonism shortly after they injected themselves with a new synthetic heroin

Answer 60

1) if impacts quality of life: Levodopa combined with DOPA decarboxylase inhibitors e.g. carbidopa, benserazide (stop L-dopa breakdown). Usually a preparation e.g. Madopar 1) if little impact on quality of life: Non-ergot derived dopamine agonist e.g. ropinirole, pramipexole, rotigotine (transdermal patch), apomorphine (can be used as infusion for major motor fluctuations) OR a Levodopa preparation OR MAO-B inhibitor e.g. selegiline, rasagiline, safinamide (protects residual dopamine against oxidation) 2) Patients w moto complications despite optimal Levodopa: - non-ergot derived dopamine agonist - MAO-B inhibitor - COMT inhibitor e.g. entacapone, tolcapone (used in combination w L-dopa to enhance its effects) -Anticholinergic compounds e.g. procyclidine, orphenadrine (as dopamine losee leads to hyperactivity of cholinergic cells) 3) If dykinesia persists DESPITE optimal Levodopa: + Amantidine 4) depression- Citalopram, sertraline or Mirtazapine (if insomniac) psychosis- quetiapine, if ineffective clozapine

Answer 61

A thalamotomy (more effective for tremors) procedure involves creating a lesion in the Vim (ventral intermediate nucelus of the thalamus) areas and this can help with tremor symptoms due to Parkinson's disease or to essential tremor among disorders Thalamotomy used for: - Severe tremors that do not respond to medication. - Less effective for bradykinesia (slowness) or rigidity. - Usually performed unilaterally (on one side) to avoid speech and cognitive side effects. Pallidotomy (more effective for dyskenesia)– lesion made and scar forms on Globus Pallidus internus (or GPi) part of basal ganglia Used for: - Reducing dyskinesia (involuntary movements) caused by levodopa. - Improving rigidity and bradykinesia. - Can help with some tremor symptoms but is less effective than thalamotomy for tremors. - Typically performed on one side, but bilateral pallidotomy is risky due to cognitive side effects. Thalamotomy → Best for tremors. Pallidotomy → Best for dyskinesia, rigidity, and bradykinesia.

Answer 62

With 130 Hz as the default stimulation frequency, most patients are treated with DBS pulses between 60 and 200 H

Answer 63

To remember the clinical features of cerebellar disease the word DANISH may be helpful: D=dysdiakdochokinesis (DDK) refers to the inability to perform coordinated, rapid muscle movements A= Ataxia (Uncoordinated, wide-based gait) N=nystagmus ( Involuntary eye movements) I= intention tremor (Tremor during purposeful movements) S= scanning dysarthria (slurred/scanning speech) H=heel-shin test; How Is the Test Performed? The patient is asked to place the heel of one foot on the opposite shin and slide it down in a straight line to the ankle. The test is repeated on both sides. 2. What Does an Abnormal Heel-Shin Test Indicate? Cerebellar Ataxia: Unsteady, jerky, or wavering movements instead of a smooth downward motion. Inability to keep the heel on the shin or overshooting the target. Seen in cerebellar lesions, particularly affecting the spinocerebellar pathways. Sensory Ataxia (due to proprioceptive loss, e.g., peripheral neuropathy): The test worsens when eyes are closed, as the patient relies on vision to compensate for lost proprioception. n.b. not to be confused with babinski test; Babinski sign is typically negative because the cerebellum does not directly control motor pathways but affects coordination and tone.

Answer 64

1. Resting Tremor; (i.e. tremor at rest) occurs when muscles at rest; disappears with voluntary movement. -Most noticeable when the limb is fully supported (e.g., resting hands on a lap). -"Pill-rolling" tremor (thumb and fingers move rhythmically). -Typically asymmetrical (starts on one side). Causes: Parkinson’s disease 2. Postural Tremor;(i.e. tremor arm up) occurs when holding a position against gravity, such as keeping arms outstretched. - Tremor appears when maintaining a posture but not at rest. - Fine, rapid shaking (6-12 Hz frequency). Causes: - Essential Tremor (most common cause; familial, improves with alcohol). - Physiological tremor (normal response to stress, anxiety, caffeine, or fatigue). -Hyperthyroidism, medication-induced tremors (e.g., beta-agonists, lithium). 3. Intention Tremor (aka Cerebellar Tremor); (i.e. tremor writing) occurs during voluntary movement, especially as the limb approaches a target. - Absent at rest but worsens near the end of movement (e.g., finger-to-nose test). - Slow, low-frequency tremor (2-4 Hz). -Often accompanied by ataxia, dysmetria, and slurred speech (cerebellar dysfunction signs). Causes: Cerebellar disorders (stroke, multiple sclerosis, tumor, alcohol-induced ataxia). Brainstem lesions affecting cerebellar output.

Answer 65

-zona incerta (targets tremor) - subthalamic nucleus (targets tremor) - globus pallidus interna (targets dystonia + tremor) n.b. DBS will not work in 'burnt out' patient with no dopamine neurones left to act one; so you need to do it whilst they're still levodopa responsive

Answer 66

Vascular Parkinsonism (VP) is parkinsonism caused by cerebrovascular disease, particularly small vessel ischemic damage to the basal ganglia and subcortical white matter. It mimics idiopathic Parkinson’s disease (PD) but has distinct clinical and radiological features. onset: - sudden or stepwise worsening after strokes unlike in Parkinson's disease where it's a gradual progression tremor: -rare or mild gait: -early gait disturbance response to levodopa: poor or minimal response - Caused by multiple small strokes or chronic ischemia affecting the nigrostriatal pathway (dopamine pathways involved in movement). - Hypertension, diabetes, smoking, hyperlipidemia, atrial fibrillation - Previous stroke or transient ischemic attacks (TIAs)

Answer 67

intentional tremor

Answer 68

- accurate symptom assessment - so electrodes are placed correctly as medications mask tremors - reduces risk of dyskinesia (involuntary movements; side effect of long-term levodopa use) as obvi this could jolt the patient move electrode

Answer 69

Tremor; levodopa is not good with treating tremor. DBS is good for treating tremor

Answer 70

Tourette Syndrome= thalamic centromedian/ parafascicular complex Treatment Resistant Depression (TRD)= Brodmann area 25 (Subcallosal cingulate white matter, nucleus accumbens) Anorexia= hypothalamus Addiction= nucleus accumbens Alzheimer's disease= anterior of the fornix OCD= nucleus accumbens, ventral striatum Obesity= hypothalamus, nucleus accumbens

Answer 71

cerebellum is found in the posterior cranial fossa

Answer 72

The cerebellum is involved in sensorimotor co-ordination - does NOT initiate movement but detects 'motor errors' - 'fine tunes' motor commands The cerebellum coordinates movement, posture, balance, eye control, and speech

Answer 73

cerebellar damage produces -instability + errors in voluntary movement - extraocular muscles affected causing nystagmus - gait change ; they open legs to compensate deficit in balance (cerebellar ataxia) N.B. cerebellar cortex exhibits neuronal plasticity; so partial recovery of function after injury is possible HOWEVER damage to deep nuclei causes persisting disability

Answer 74

Ataxia is a loss of muscle control

Answer 75

the vestibulocerebellum is made up of nodulus + flocculus

Answer 76

cerebrocerebellum/ neocerebellum= planning + execution of high skilled movements, temporal sequences + speech injury to cerebrocerebellum/ neocerebellum= dysmetria (inability to judge distances), INTENTION TREMOR, dysarthria (slurred, slow speech as a result of impaired muscle control), dysdiadochokinesis (inability to perform rapid, coordinated movements) spinocerebellum= coordination of distal movements (lateral + paramedian) + proximal movements + eye movements (vermis) injury to spinocerebellum= ataxic gait, hypotonia, pendular reflexes vestibulocerebellum= vestibulo-ocular reflex, posture + equilibrium injury to vestibulocerebellum= vertigo ('spinning feeling' of dizziness), nystagmus, ataxic gait

Answer 77

Tentorium Cerebelli; A fold of dura mater that forms a horizontal partition between the cerebellum (below) and the occipital lobes of the cerebrum (above)

Answer 78

the anterior lobe of cerebellum is separated from the posterior lobe by the PRIMARY FISSURE the posterior lobe of cerebellum is separated from the floculo-nodular lobe by the POSTERIOR LATERAL FISSURE

Answer 79

vermis= head, neck + trunk (axial) intermediate zones (aka paravermal areas)= upper and lower limbs

Answer 80

dentate nucleus is found in the lateral hemispheres in the posterior lobe of the cerebellum The dentate nucleus is the largest and most lateral of the 4 deep cerebellar nuclei (Fig 2). The emboliform and globose nuclei, collectively referred to as the interposed nuclei, are positioned more medially, and the fastigial nucleus lies adjacent to the midline.

Answer 81

hemiballismus describes wild, flinging limb movements usually caused by a small infarct in the sub-thalamic nucleus

Answer 82

This facial nerve has a course that goes from the pons, through the internal acoustic meatus of the temporal bone together with vestibulocochlear nerve (B), and then exits the skull via the stylomastoid foramen.

Answer 83

The main blood supply to the basal ganglia comes from lenticulostriate arteries which are branches of the middle cerebral artery (MCA), which is a continuation of the internal carotid artery.

Answer 84

The vestibular system detects head movements through specialized structures in the inner ear: * Angular Acceleration: Detected by the semicircular canals. Each canal is oriented perpendicularly to the others, corresponding to the three spatial planes. When the head rotates, endolymph fluid within these canals moves, causing deflection of the cupula and bending of hair cells. This mechanical deformation transduces angular motion into neural signals. * Linear Acceleration: Detected by the otolith organs (utricle and saccule). These structures contain hair cells embedded in a gelatinous matrix with calcium carbonate crystals (otoconia) on top. Linear movements or gravitational forces cause displacement of the otoconia, leading to bending of the hair cells and conversion of linear acceleration into neural signals.

Answer 85

Vestibulo-Ocular Reflex/VOR; Head turn → Vestibular nuclei → MLF → CN VI (lateral rectus) + CN III (medial rectus) → Eyes move opposite to head turn. VOR ensures gaze stabilisation for clear vision during movement. nystagmus: involuntary, rhythmic eye movements, typically comprising a slow phase (drift) in one direction followed by a quick, corrective phase in the opposite direction. It can occur physiologically (as a response to sustained rotation) or pathologically due to VOR dysfunction.

Answer 86

Vestibular dysfunction can manifest through various symptoms, including: - Vertigo: A sensation of spinning or motion - Nystagmus: Involuntary eye movements - Postural Instability: Unsteady gait and balance issues - Nausea and Vomiting: Often accompanying vertigo - Intolerance to Head Movements: Discomfort or dizziness with head motion These symptoms can result from peripheral causes (e.g., benign paroxysmal positional vertigo) or central causes (e.g., ischemic stroke in the posterior fossa

Answer 87

- Head Impulse Test: Assesses the VOR by observing the ability to maintain gaze on a target during rapid head movements. - Dix-Hallpike Maneuver: Diagnoses benign paroxysmal positional vertigo by observing nystagmus and vertigo in response to specific head positions. - Romberg Test: Evaluates postural stability by having the patient stand with feet together, eyes closed, and assessing for swaying or imbalance. - Caloric Testing: Stimulates the vestibular system using warm or cold water or air in the ear canal to induce nystagmus, assessing unilateral vestibular function. Head turn to the right will increasing firing of the right horizontal canal and decrease firing of the left to compensate. (n.b. COWS acronym; Cold water= eyes deviate to ipsilateral ear, nystagmus beats away to Opposite ear. Warm water= eyes deviate to contralateral ear + nystagmus beats towards Same ear. - Electronystagmography (ENG) or Videonystagmography (VNG): Record eye movements to evaluate vestibular function and identify nystagmus patterns.

Answer 88

The vestibular system is a sensory system that maintains balance, posture + orientation The vestibular system detects motion, head position + spatial orientation via the eyes, general proprioceptive (muscles,joints) + cutaneous receptors, and vestibular receptors in the inner ear (vestibular apparatus)

Answer 89

Perilymph = Extracellular-like, surrounds labyrinth, absorbs vibrations. Endolymph = Intracellular-like, inside labyrinth, activates hair cells. Perilymph: Where? Scala tympani & scala vestibuli (surrounds membranous labyrinth). Ions? High Na⁺, Low K⁺ (like CSF/plasma). Function? Cushions & transmits sound to cochlea. Made by? CSF & blood plasma (via cochlear aqueduct). Endolymph: Where? Scala media & membranous labyrinth (inside semicircular canals, utricle, saccule). Ions? High K⁺, Low Na⁺ (like intracellular fluid). Function? Drives hair cell activation for hearing & balance. Made by? Stria vascularis (cochlea) & dark cells (vestibular system).

Answer 90

Ductus Reuniens is the structure that joins the auditory labyrinth (cochlea) to the vestibular labyrinth. Ductus Reuniens: Function: Connects the scala media (cochlear duct) of the cochlea to the saccule in the vestibular system. Location: A narrow membranous duct within the endolymphatic system. Role: Allows endolymph to flow between the cochlea and vestibular system, maintaining the ionic balance necessary for both hearing and balance.

Answer 91

GLUTAMATE is released when hair cells depolarise in ampullae of semicircular ducts

Answer 92

Benzodiazepines (e.g., diazepam, lorazepam, clonazepam) are prescribed for vestibular lesions because they suppress vestibular activity= reducing symptoms like vertigo, dizziness, and nystagmus. Benzodiazepines (BZDs) are GABA-A receptor agonists (bind to BZD site on GABA-A receptor). Increased GABA activity dampens abnormal vestibular signals, reducing the hyperactivity caused by vestibular imbalance

Answer 93

Parieto-Insular Vestibular Cortex (PIVC) (core vestibular processing) Retroinsular Cortex (Ri) (integrates otolith & semicircular canal signals) Parietal Operculum (OP2) (human vestibular area, visual-vestibular integration) Posterior Insular Cortex (PIC) (vestibular and visual input processing) Temporo-Parietal Junction (TPJ) (multisensory integration) Cingulate Sulcus Visual Area (CSv) (self-motion perception) Precuneus Motion Area (PcM) (visual-vestibular coordination) V6 Complex (visual motion & spatial awareness)

Answer 94

1. Transduction(ion channels): noxious (potentially harmful) stimuli translated into electrical activity at sensory nerve endings 2. Transmission (neurones): propagation of impulses along pain pathways 3. Perception (brain pain matrix): discrimination/ affect/ motivation 4. Modulation: Positive + negative modulation occurs

Answer 95

- Capsaicin receptor TRPV1 channel is a non-selective cation channel that is activated by temperature, acid, capsaicin + mustard/wasabi - TRPM8 ion channel (cold and menthol receptor 1) is activated by cold temperature + cooling agents (menthol) - Acid-sensing ion channel (ASIC) is a cation channel activated by pH changes Remember as: She’s hot, she’s V1 (the one) (TRPV1) Are cool (8), m8? (TRPM8)

Answer 96

- A beta (most myelinated) - A delta (less myelinated) - C fibres (unmyelinated)

Answer 97

Myelinated A delta fibres carry '1st pain' a sharp, stinging, pricking vs Unmyelinated C fibres carry '2nd pain', a diffuse + persistent burning pain N.B. speed of transmission is dependent on myelination + axon diameter (faster if myelinated + wider diameter cuz less resistance to flow)

Answer 98

- Congenital insensitivity to pain (CIP)= caused by loss of function mutations in Nav1.7 (sodium channel subunit) THEY FEEL NO PAIN rare condition in which individual cannot feel pain so often have wounds, broken bones, health issues not detected - Inherited erythromelalgia (IE)= caused by gain of function mutations in Nav1.7 channel (sodium channel subunit) HYPERSENSITIVE TO PAIN; it's a painful neuropathy involving severe chronic burning pain sensations in hands + feet

Answer 99

- Congenital insensitivity to pain with anhidrosis (CIPA)= mutation in TRKA gene encodes neurotrophic receptor tyrosine kinase 1 (TrkA receptor) for nerve growth factor (NGF); NGF support survival of nociceptive sensory neurones in DRG so these patients lack NGF-dependent A delta + C fibres - Diabetic neuropathy= high blood glucose damages the nerve fibres especially in legs + feet (ex. painful)

Answer 100

- limbic system= subjective sensations of pain + pleasure - intralaminar (reticular) nuclei of thalamus= induced arousal + descending control of nociceptor input - periaqueductal grey (PAG)= descending pain modulation - reticular formation= alerting cerebral cortex + focus of attention on pain

Answer 101

processes underlying pain perception involve primarily the thalamus and cortex, however the others also play roles - anterior cingulate cortex (ACC)= emotional reaction/ motivation - pre-frontal cortex= evaluation/ cognition - insula= 'pain' map, interoception, homeostatic adjustment, emotion - primary sensory cortex= somatosensory, discrimination-location intensity - amygdala= aversion; emotional memory + response

Answer 102

- allodynia= a condition where pain is caused by a non-noxious (non-painful) stimulus (e.g. tickle with a feather) - hyperalgesia= a condition where an abnormal increased pain sensitivity is caused by noxious (painful) stimulus (e.g. hot water on sunburn) - peripheral sensitisation= an increased sensitivity to afferent nerve stimuli at the peripheral site - central sensitisation= an increased sensitivity to an afferent nerve stimuli at the CNS site

Answer 103

Premotor cortex

Answer 104

Substantia nigra pars compacta Dopaminergic neurons in the SNpc project to the striatum, forming the nigrostriatal pathway, which plays a critical role in the modulation of voluntary movements

Answer 105

DOPA decarboxylase inhibitors= Benserazide, Carbidopa, work by inhibiting the enzyme aromatic L-amino acid decarboxylase (DOPA decarboxylase), which is responsible for converting L-DOPA into dopamine in peripheral tissues (you want the dopamine in brain not peripheral tissues; hence this reduces bad side effects and means u can lose the L-DOPA at lower dose) Common formulations with Levodopa: Carbidopa/Levodopa (Sinemet) Benserazide/Levodopa (Madopar

Answer 106

Carbamazepine (anticonvulsant + mood stabiliser) mechanism of action: - Sodium Channel Blockade: Carbamazepine stabilizes sodium channels in neurons, reducing excessive neuronal firing. This action may help control movement abnormalities in HD -Neurotransmitter Modulation: It affects neurotransmitter systems, including dopamine and glutamate, which are involved in HD. This modulation may help alleviate symptoms related to dopamine dysregulation and limit excitotoxicity.

Answer 107

Purkinje cells

Answer 108

locus coeruleus in the brainstem region that contains noradrenergic neurons producing analgesia in a fight-or-flight situation

Answer 109

pregabalin

Answer 110

The first-line drugs for neuropathic pain are: - SNRIs (Duloxetine, Venlafaxine) - TCAs (Amitriptyline, Nortriptyline) - Ca2+ channel ligands (Gabapentin, Pregabalin)

Answer 111

Intravenous

Answer 112

anterior cerebral artery supplies corpus callosum

Answer 113

basilar artery supplies the pons

Answer 114

lacunar stroke

Answer 115

Contrecoup

Answer 116

Broca's area

Answer 117

Eyeopening, verbal and motor responses

Answer 118

Episodic memory= a type of long-term memory that involves conscious recollection of previous experiences together with their context in terms of time, place, associated emotions, etc.

Answer 119

Subgenual cingulate cortex is associated with sadness

Answer 120

Operant conditioning

Answer 121

Classical conditioning

Answer 122

Transporter

Answer 123

Dorsolateral prefrontal cortex

Answer 124

endogenous agent= respond to neurotransmitters, hormones and cytokines exogenous agent= respond to drugs

Answer 125

Seizures = Abnormal, paroxysmal changes in the electrical activity of the brain; they reflect large-scale synchronous discharges of neuronal networks Epileptogenesis = The process by which normal brain function progresses towards generation of abnormal electrical activity Epilepsy = A neurological disorder that represents a brain state that supports recurrent, unprovoked seizures – it has neurobiological, cognitive, psychological, and social consequences

Answer 126

Status Epilepticus = A form of epilepsy which is a life-threatening medical emergency. Seizures which last more than 5 minutes (or more than 1 seizure in 5 minutes without regaining consciousness). 3 types: Generalized Onset = They affect both sides of the brain from the onset. The networks affected can be cortical or subcortical. Focal Onset = They start in an area or network in one of the brain hemispheres. The networks affected can be cortical or subcortical. They can remain localized or spread to large areas. They can also be described with the term partial seizures. Unknown Onset = Seizures are classified in this category if the beginning of the seizure is uncertain. During clinical evaluation, it may become possible to change the classification into either generalized or focal onset seizure.

Answer 127

- reorganisation of hippocampal tissue in temporal lobe epilepsy - loss of chandelier cells (increases the risk of abnormal excitatory activity); a specific population of interneurons which are GABAergic cells that control the activity of cortical pyramidal cells; they synase on the axon initial segment of pyramidal cells

Answer 128

1) abnormal neuronal excitability (ion channels) 2) decreased neuronal inhibition (GABA-dependent) 3) Increased neuronal excitation (glutamate-dependent) n.b. neurones in an epileptic focus have burst firing profiles, which reflect abnormal fluctuations in membrane voltage; the 'paroxysmal depolarising shift' phenomenon; a particular role for NMDA glutamate receptors in the depolarising plateau other causes: - glial abnormalities

Answer 129

mTOR pathway is a major regulator of growth + homeostasis REST pathway leads to negative regulation of the expression of many genes in CNS

Answer 130

1. Generalised Tonic-Clonic Seizures (formerly known as Grand Mal Seizures): Description: These seizures involve a loss of consciousness and violent muscle contractions, affecting the entire body Tonic- stiffness (muscle rigidity) Clonic- rhythmic jerking movements (repetitive muscle contractions) First-Line: Lamotrigine as monotherapy. Alternative Options: If lamotrigine is unsuitable/not tolerated, consider carbamazepine or oxcarbazepine. 2. Absence Seizures (formerly known as Petit Mal Seizures): Description: Characterised by brief, sudden lapses in attention and activity, often mistaken for daydreaming. First-Line: Ethosuximide as monotherapy. Alternative Options: If ethosuximide is unsuitable or not tolerated, consider lamotrigine. (Memory tip: absence seizures u ‘lose ur ethos’ - 1st line is ethosuximide’

Answer 131

3. Focal Seizures: Description: Seizures originating in a specific area of the brain, with symptoms varying depending on the affected region. First-Line Treatment: Offer carbamazepine or lamotrigine as monotherapy. Alternative Options: If the first choice is unsuitable or not tolerated, consider levetiracetam, oxcarbazepine, or sodium valproate. 4. Myoclonic Seizures: Description: Involve sudden, brief jerks or twitches of a muscle or group of muscles. First-Line Treatment: Offer sodium valproate as monotherapy. Alternative Options: If sodium valproate is unsuitable or not tolerated, consider levetiracetam or topiramate.

Answer 132

5. Tonic or Atonic Seizures: Description: Tonic seizures involve sudden muscle stiffening, while atonic seizures involve sudden loss of muscle tone, often leading to falls. n.b. both treated the same First-Line Treatment: Offer sodium valproate as monotherapy. Alternative Options: If sodium valproate is unsuitable or not tolerated, consider lamotrigine.

Answer 133

How carbamazepine can worsen absence seizures: Absence seizures are primarily caused by abnormal activity in T-type calcium channels in the thalamus. Drugs like ethosuximide and sodium valproate work by blocking these calcium channels. Carbamazepine does not inhibit T-type calcium channels and can actually increase burst firing in the thalamus, leading to worsening of absence seizures. How carbamazepine worsens myoclonic seizures: Myoclonic seizures involve sudden muscle jerks due to cortical hyperexcitability. Carbamazepine can paradoxically increase excitability in certain neuronal circuits, leading to increased myoclonic jerks.

Answer 134

chronic pain is pain that has been present for more than 12 wks (3 months), and that lasts beyond tissue healing

Answer 135

(function) The raphe nuclei of the brainstem provide the major source of serotonergic neurons in the central nervous system (location) The raphe nuclei are positioned midline in the brainstem throughout the midbrain, pons, and medulla

Answer 136

pain= subjective experience nociception= bodies ability to detect changes in environment (noxious stimuli i.e. potentially harmful stimuli) 1) transduction 2) transmission 3) perception 4) pain modulation

Answer 137

Non-steroidal anti-inflammatory drugs inappropriate in patients with - asthma - renal impairment - heart disease - uncontrolled hypertension - peptic ulcers

Answer 138

proton pump inhibitors e.g. omeprazole, lansoprazole

Answer 139

- constipation - skin itching (PRURITIS) - nausea - altered mental status - respiratory depression

Answer 140

Damage to the corpus callosum severs communication between the cerebral hemispheres

Answer 141

The mammillary bodies are involved in recollective memory/ storage of episodic daily memory (memories associated with daily events).

Answer 142

chronic primary pain; - ANTIDEPRESSANTS - DO NOT GIVE ANALGESIA unless its an antidepressant

Answer 143

scored out of 10 4 or more= it's neuropathic pain first-line: - amitriptyline (TCA) - duloxetine (SNRI) - gabapentin (anticonvulsant) - pregabalin (anticonvulsant) N.B. ONLY 1 MED CAN BE USED AT A TIME other options: - tramadol (short term relief) - capsaicin cream (localised areas) - physiotherapy - psychotherapy

Answer 144

trigeminal neuralgia= (type of extreme pain) sudden, paroxysmal attacks of pain: electric shock-like, sharp, stabbing, usually unilateral (lasts few secs to few min) site: cheekbone, nose, upper lip, upper teeth, sometimes extended to lower lip, teeth, chin most common cause: compression, distortion or stretching of the nerve V root fibres by a branch of anterior or posterior inferior cerebellar artery first-line: carbamazepine (blocks sodium channels)

Answer 145

Cachexia is a complex metabolic syndrome characterized by involuntary weight loss, muscle atrophy, and systemic inflammation often seen in people chronic illnesses. (doesn't improve with nutrition) Most common in diseases like cancer, congestive heart failure, chronic obstructive pulmonary disease, chronic kidney disease, and AIDS

Answer 146

The brain receives 15% of cardiac output + used 20% of o2 + 25% of total glucose av. brain blood flow= 46mL/100 grams

Answer 147

20 secs of anoxia leads to unconcsciousness >5min permanent unconsciousness + neuron death

Answer 148

Presentation of Third Nerve Palsy: - 'Down & Out' Eye Position → due to unopposed actions of the lateral rectus and superior oblique. - Ptosis (Drooping Eyelid) → due to loss of innervation to levator palpebrae superioris. - Mydriasis (Pupillary Dilatation) → due to loss of parasympathetic innervation to sphincter pupillae. n.b. Occulomotor (CN III) Origin: oculomotor nucleus in the midbrain of the brainstem. Course: Emerges from the anterior aspect of the midbrain. Travels through the cavernous sinus before entering the orbit via the superior orbital fissure. Motor Supply: Extraocular muscles: Superior rectus Medial rectus Inferior rectus Inferior oblique Levator palpebrae superioris (raises the upper eyelid). Parasympathetic Supply: Preganglionic fibres originate in the Edinger-Westphal nucleus. Postganglionic fibres arise from the ciliary ganglion to innervate: Sphincter pupillae → causing pupillary constriction (miosis) Ciliary muscles → for lens accommodation

Answer 149

Hemiparesis is one-sided muscle weakness

Answer 150

Left middle cerebral artery infarctions typically result in contralateral hemiparesis, contralateral hemisensory deficit, and aphasia. Infarcts that involve Broca's area result in expressive aphasia.

Answer 151

arachnoid granulations allow CSF to flow into venous blood of sinuses but prevent backflow of blood into SUB-ARACHNOID SPACE

Answer 152

58% population have RIGHT dominant transverse sinus

Answer 153

major causes of haemorrhagic stroke: - hypertension - aneurysm - elderly - head injury (trauma) - alcoholics - arteriovenous malformation

Answer 154

TIA= a transient episode of neurologic dysfunction caused by focal brain, spinal cord, or retina ischemia, without acute infarction symptoms if anterior circulation: - motor weakness - hemi-sensory loss - dysarthria - transient monocular blindness symptoms if posterior circulation: - vertigo - diplopia - ataxia - amnesia

Answer 155

Epidural (extradural) hematoma - Traumatic - Blood between dura mater and the skull - Bleeding rapid (arterial*) - Mortality 10% - May present with lucid period immediately after trauma followed by unconsciousness - Bleed rapid arterial (or large venous sinuses) e.g. Middle meningeal A. (temperoparital area, pterion) e.g. Ant. Ethmoidal A. (frontal) Symptoms: - As blood collects it compresses intracranial structures - Compress CN III - Weakness of extremities on opposite side of lesion (crossed pyramid pathways) - Loss of visual field opposite to lesion (compress of PCA) Diagnosis: - CT or MRI Convex lens (biconvex, hyperdensity) - Expansion stops at the sutures because dura is more tightly attached here - then presses inwards

Answer 156

Subdural hematoma - Traumatic / Ageing (Chronic) - Blood between dura mater and arachnoid mater - Rupture to bridging veins Acute 12-29% of severe TBI - Mortality 40-60% can be Acute, subacute or chronic Acute after high-speed acceleration and deceleration - Associated with cerebral contusions - Slower onset as venous bleed - Chronic – previous head injury Symptoms: - Irritability - Seizures - Headache - Numbness - Disorientation Diagnosis: - CT scan - Crescent shaped, concave Hyperdense = acute, hypodense = chronic They cross the suture lines

Answer 157

Subarachnoid hematoma - Spontaneous - Between arachnoid and pia - Ruptured aneurysm or head injury - 1-7% of strokes - Arterial - Most frequent traumatic brain lesion Symptoms: - Severe headache (thunderclap) - Vomiting - Confusion - Lowered / fluctuating levels of consciousness Diagnosis: - CT - White signal diffuse over sulci on both sides - Intraventricular hyperdensities (aka bleeding into ventricles) - Lumbar puncture - Evidence of blood in 3% of people with normal CT - Also bilirubin; CSF will be xanthochromic in victim N.B. ECG resembles a STEMI (40-70% of cases)

Answer 158

in greek means yellow Xanthochromia is the observation of a yellowish discoloration in cerebrospinal fluid (CSF) attributed to the presence of bilirubin

Answer 159

TYPES: - Saccular (berry is a sub-type)= is a rounded sac containing blood, that is attached to a main artery or branches; BERRY is most common form of cerebral aneurysm. It is typically found on arteries at the base of the brain. - Fusiform= balloons or bulges out on all sides of the artery. - Mycotic= occurs as the result of an infection that can sometimes affect the arteries in the brain. The infection weakens the artery wall, causing a bulging aneurysm to form. - 1:15 people develop a brain aneurysm -Women at higher risk 3:2 -Danger comes if it ruptures (i.e. becomes subarachnoid hemorrhage) - tend to form at junction points where arteries are dividin

Answer 160

A hemorrhagic transformation (HT) of an infarct is a complication of ischemic stroke in which bleeding occurs into the area of brain tissue that was previously deprived of blood supply. It is a spectrum that ranges from small petechial hemorrhages to large, space-occupying hematomas. 2 types of hemorrhagic transformation (HT) of an infarct: 1) Hemorrhagic infarction (HI) – Small, scattered bleeding within the stroke area. 2) Parenchymal hemorrhage (PH) – Larger, more severe bleeding that may cause brain swelling.

Answer 161

primary cause= hypertension secondary causes= trauma, tumour, arteriovenous malformations, venous thrombosis, vasculitis, coagulopathy, drugs e.g. cocaine, hemorrhagic transformation of infarct complications of ICH: - local damage - local mass effect/ herniation - raised ICP (intracranial pressure) - hydrocephalus

Answer 162

1. Vascular Occlusion 💡 Cause: Blockage in a cerebral artery (thrombus or embolus). 🔴 Effect: Reduced blood flow to the brain. 2. Energy Failure 💡 Cause: Lack of oxygen & glucose. 🔴 Effect: ATP production stops, neurons can't function properly. 3. Ion Imbalance 💡 Cause: ATP loss disrupts ion pumps. 🔴 Effect: Sodium & calcium build up inside cells, leading to depolarization. 4. Glutamate Release 💡 Cause: Depolarization triggers excess glutamate release. 🔴 Effect: Overstimulation of neurons. 5. Excitotoxicity 💡 Cause: Glutamate overactivates NMDA & AMPA receptors. 🔴 Effect: Too much calcium enters neurons, damaging them. 6. Oxidative Stress 💡 Cause: Mitochondria dysfunction, producing reactive oxygen species (ROS). 🔴 Effect: Cell damage from oxidative stress. 7. Cell Death 💡 Cause: Neurons die from lack of energy & toxic buildup. 🔴 Effect: Brain tissue damage (necrosis & apoptosis). 8. Inflammatory Response 💡 Cause: Dying cells release inflammatory signals. 🔴 Effect: Immune response worsens brain injury. 📌 Summary: Blocked blood flow → Energy failure → Ion imbalance → Excitotoxicity → Cell death → Inflammation → Brain damage

Answer 163

Arteriosclerosis (general term) Refers to the hardening and thickening of arterial walls due to aging, high blood pressure, or other factors. Can occur in any artery in the body. Leads to reduced elasticity of the arteries, making it harder for blood to flow. Atherosclerosis (specific type of arteriosclerosis) A subtype of arteriosclerosis caused by the buildup of fatty plaques (cholesterol, fats, and other substances) inside the arteries. Mainly affects medium and large arteries like the coronary and carotid arteries. Can lead to blockages, increasing the risk of heart attacks and strokes.

Answer 164

Lacunar infarcts are common in the subcortical deep brain structures, including the thalamus, basal ganglia, pons, and white matter of the internal capsule. n.b. Lacunar infarcts can be asymptomatic and are noted on imaging as incidental findings.

Answer 165

Hemianopia means a person loses half of their visual field in one or both eyes

Answer 166

Anterior circulation (ACA)= unilateral motor deficit, homonymous hemianopia, - left side/dom side= dysphasia - right side/non-dom side= neglect syndrome Posterior circulation (PCA)= pure hemianopia (half-blindness or blinding) Lacunar (small vessel strokes)= pure motor (50%), pure sensory (5%), ataxic hemiparesis (10%)= poor muscle control (ataxia) and incomplete paralysis (paresis), sensorimotor stroke (35%)

Answer 167

📌 Prothrombin Fragment 1+2 (F1+2) 💡 Indicator: Increased thrombin generation. 🔍 Use: Suggests higher blood clotting activity. 📌 Inflammatory Markers (CRP, IL-6) → May indicate stroke risk. 📌 D-dimer → Elevated in stroke due to clot breakdown. 📌 Glucose Levels → High levels can worsen stroke severity.

Answer 168

1. Rapid Recognition & Diagnosis ✅ FAST Test → Identify symptoms (Face, Arm, Speech, Time). ✅ Exclude Hypoglycaemia → Rule out low blood sugar. ✅ Emergency Assessment → Use ROSIER tool in hospital.

Answer 169

1. Onset of Symptoms Ischaemic: Gradual, develops over time. Hemorrhagic: Sudden, quick onset. 2. Headache Ischaemic: Rare, not a key symptom. Hemorrhagic: Severe, sudden headache ("thunderclap"). 3. Neurological Deficits Ischaemic: Weakness, numbness, or speech problems on one side. Hemorrhagic: Similar deficits + nausea, vomiting, or confusion. 4. Consciousness Ischaemic: Usually remains conscious at first. Hemorrhagic: Rapid loss of consciousness or confusion. 5. Nausea and Vomiting Ischaemic: Rare. Hemorrhagic: Common due to brain pressure. 6. Seizures Ischaemic: Rare. Hemorrhagic: More common, linked to bleeding. 📌 Quick Recap: Hemorrhagic = Sudden, severe headache, nausea, loss of consciousness. Ischaemic = Gradual symptoms, weakness, speech problems.

Answer 170

Rapid blood pressure lowering treatment should not be given to patients who have an underlying structural cause, have a score on the Glasgow Coma Scale of below 6, are going to have early neurosurgery to evacuate the haematoma, or who have a very large haematoma with a poor expected prognosis.

Answer 171

dysarthria= disorder affecting articulation dysphonia= voice disorder dysarthrophonia= voice + articulation disorder (in all of these language and cognition is normal)

Answer 172

Acquired aphasia (aka dysphasia) you 'acquire' it doesn't worsen over time e.g. Broca's, Wernicke's Progressive aphasias are caused by a gradual degeneration of brain tissue due to neurodegenerative diseases like: - Primary Progressive aphasia (PPA)= (can be semantic, logopenic, nonfluent agrammatic) it's a a subtype of frontotemporal dementia - Semantic Dementia (SD)= A semantic subtype of Primary Progressive Aphasia (PPA) which is characterized by progressive loss of word meaning and difficulty recognizing objects or familiar faces. Patients may still speak fluently but use nonspecific or incorrect words. Caused by degeneration of the anterior temporal lobe

Answer 173

logopenic variant PPA (lvPPA)= Word-finding difficulty (long pauses but proper grammar) nonfluent agrammatic PPA (nfaPPA)= Speech production issue (grammar & fluency) semantic variant PPA (svPPA)= Loss of word meaning (difficulty understanding words)

Answer 174

- difficulty remembering words (ANOMIA) - saying the wrong words (PARAPHASIAS) - difficulty forming sentences (TELEGRAMMATISM) - difficulty understanding speech (word sound/meaning deafness - reading + writing problems (acquired dyslexia/ dysgraphia) - problems with numbers (dyscalculia)

Answer 175

🔍 Standard Straight Leg Raise (SLR) Test - What It Assesses: Lower lumbar radiculopathy (L4-S1 nerve roots) - How It’s Performed: Patient lies supine (face up). Examiner lifts the straight leg while keeping the knee extended. - Positive result: Pain radiating down the posterior thigh and leg (sciatic nerve distribution). - Indicates: L4-S1 disc herniation Sciatic nerve irritation 🔄 Reverse Straight Leg Raise (rSLR) Test - What It Assesses: Upper lumbar radiculopathy (L2-L4 nerve roots) & femoral nerve irritation - How It’s Performed: Patient lies prone (face down). Examiner lifts the extended leg off the table (hip extension). - Positive result: Pain in the anterior thigh or lower back. - Indicates: L3-L4 disc herniation Femoral nerve entrapment Retroperitoneal pathology (e.g., tumor, abscess)

Answer 176

Peripheral neuropathy is the damage of the peripheral nervous system, such as carpal tunnel syndrome that involves trapped nerves in the wrist. Radiculopathy is the pinching of the nerves at the root, which sometimes can also produce pain, weakness and numbness in the wrist and hand

Answer 177

Lumbosacral radiculopathy occurs due to inflammation and mechanical compression of the one lumbosacral nerve roots. In the absence of red flag signs such as; thoracic pain, fever/unexplained weight loss, bowel or bladder dysfunction the first-line treatment for all radiculopathies: NSAIDs are the first line treatment for radiculopathy e.g. diclofenac, naproxen NSAIDs help to manage radiculopathy by inhibiting cyclo-oxygenase, an enzyme responsible for prostaglandin production which augments pain triggers inflammation. Inhibiting this enzyme results in analgesia and a reduction in nerve root inflammation, and so reduces symptoms.

Answer 178

primary= headache that is not caused by another medical condition. Examples include migraine, tension-type headaches, and cluster headache. secondary= A headache caused by an underlying condition (e.g., infection, injury, or disease). Examples include sinus headaches, headaches from trauma, and medication overuse headache

Answer 179

n.b NEVER TREAT HEADACHES WITH CODEINE (makes them worse) 1. Tension-Type Headache (TTH); Mild to moderate bilateral headache (feels like a tight band around the head). Not aggravated by routine activities (e.g., walking). No nausea or vomiting, but may have photophobia or phonophobia (not both). Management (NICE): Acute treatment: Paracetamol, aspirin, or NSAIDs (ibuprofen, naproxen). Prevention: Lifestyle changes (reduce stress, improve sleep, regular meals). Amitriptyline (only if frequent/chronic TTH). 2. Migraine (With or Without Aura); Unilateral, throbbing headache that worsens with activity. Associated with nausea/vomiting, photophobia, and phonophobia. Aura (if present): Visual (flashing lights, blind spots), sensory (tingling, numbness), or speech disturbances. Management: Acute treatment: First-line: Triptans (e.g., sumatriptan) + NSAIDs or paracetamol. Consider antiemetics (e.g., metoclopramide) even if no nausea. Prevention: Propranolol or topiramate (if frequent or disabling attacks). Amitriptyline as an off-label option. Lifestyle changes 3. Cluster Headache; Severe unilateral headache, usually around the eye or temple. Occurs in clusters (several times a day for weeks/months, then remission). Autonomic symptoms: Tearing, nasal congestion, eyelid swelling, ptosis, or red eye on one side . Management: Acute treatment: 100% oxygen (12–15 L/min via non-rebreather mask). Subcutaneous or nasal triptans (e.g., sumatriptan SC or zolmitriptan nasal spray). Prevention: Verapamil 240mg daily (first-line for prevention) n.b. verapamil causes gingivitis and needs ECG as dose so high. Consider short courses of prednisolone for short-term prevention.

Answer 180

1) Triggers (e.g. stress, hormones, diet) activate a genetically sensitive brain (followed with premonitory symptoms e.g. yawning/cravings which start in hypothalamus) 2) Cortical spreading depression (wave of increased and then decreased brain activity)= A wave of electrical activity spreads across the cortex. Leads to aura (if present) and activates the trigeminovascular system (TGVS). 3) Trigeminovascular system activation causing inflammation and the dilation of meningeal blood vessels resulting in pain. The trigeminal ganglion (PNS) detects signals and relays them to the spinal trigeminal nucleus caudalis (CNS). This leads to the release of CGRP (calcitonin gene-related peptide is a powerful VASODILATOR), causing vasodilation and central sensitization. 4. Signals reach the thalamus, which processes pain. - Hypothalamus may regulate attack onset and symptoms like nausea. = MIGRAINE headache

Answer 181

the phenomenon that causes aura is cortical spreading depression (CSD) - a transient + local suppression (depression) - of spontaneous electrical activity in the cortex (cortical) - moving slowly across the brain (spreading)

Answer 182

penetrating injury= foreign object (e.g. bullet) enters into brain causing focal damage closed head injury= blow to the head (e.g. road traffic accident); skull fracture, contusion (bruise), hematomas (blood clots), lacerations (tear), diffuse axonal injury (nerve damage) blast injury= explosion (e.g. bomb) create fast moving pressure wave that passes through the brain + damages axons and vasculature

Answer 183

focal injury= coup (at site), countrecoup (opposite site) diffuse injury= widespread injury, major cause of unconsciousness + persistent vegetative state

Answer 184

Glasgow coma scale assesses 3 criteria; eye opening (1-4), verbal response (1-5), best motor response (1-6). The lowest possible score is 3 (most severe), the highest score is 15 (healthy) Loss of Consciousness scale (LOC)= measures time patient was unconscious Post traumatic amnesia (PTA) scale= measures the interval from injury until patient is orientated + can form/recall new memories mild TBI/concussion; - GCS: 13-15 - LOC: <30min - PTA: <60min moderate TBI; - GCS: 9-12 - LOC: 1-24hrs - PTA: 1-24hrs severe TBI; - GCS: 3-8 - LOC: >24hrs - PTA: >24hrs

Answer 185

all unconscious patients require a CT scan to HEAD and C-spine

Answer 186

normal adult ICP: 5-15mmHg (supine position) Monro-Kellie Hypothesis: - ICP is a pressure-volume relationship - brain enclosed in a fixed non-expandable skull - increase in mass (hematoma) reduces CSF + cerebral blood flow in the brain - decrease in brain blood + CSF causes ischaemia + brain cell death - INCREASE ICP can cause herniation a mass with an ICP ≥20mmHg

Answer 187

These both can occur on one or both sides of the body Decorticate posture: damage to cerebral cortex and or internal capsule. features: arms adducted + flexed, arms at CORE (middle of body), legs internally rotated + feet plantar flexed Decerebrate posture: damage to midbrain, brainstem and/or pons. features: arms adducted + extended pronation (side by side) + feet plantar flexed

Answer 188

n.b. epi= above sub= below intra= within 1. Epidural Hematoma (EDH) 2. Subdural Hematoma (SDH) 3. Subarachnoid Hematoma (SAH) 4. Intracerebral Hematoma (ICH)

Answer 189

Pupil dilation is thought to be the result of UNCAL herniation causing mechanical compression of the IIIrd cranial nerve and subsequent brain stem compromise. However, not all patients with herniation have fixed and dilated pupils, and not all patients with nonreactive, enlarged pupils have uncal herniation Uncal herniation most typically results in a CN III palsy, producing the characteristic 'down and out' appearance of the eye on the affected side.

Answer 190

middle meningeal artery epidural hematoma is a blood clot between skull and outer layer of dura (endosteal layer) - CT lemon

Answer 191

Subdural hematoma is mostly from damage to bridging cortical veins Subdural hematoma is a blood clot in the subdural space between the dura + arachnoid mater of the meninges - CT banana

Answer 192

Subarachnoid hematoma (SAH)= blood clot in subarachnoid space between arachnoid + pia of meninges SAH is more common from damage in cerebral sulci

Answer 193

premotor cortex

Answer 194

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