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Anatomy: several systems (Jenna Goff) > Neuro anatomy > Flashcards

Neuro anatomy Flashcards

1
Q

What is meant by the dominant and non-dominant cerebral hemispheres?

A

the side of the brain that controls writing and speech is called the dominant hemisphere
the L hemisphere is dominant in over 90% of right handed people, and 60% of left handed people

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2
Q

What is the function of the prefrontal cortex area of the frontal lobe? What are the symptoms of a lesion in this area?

A

the anterior and orbital parts of the frontal cortex govern personality, emotional expression, initiative and the ability to plan

altered behaviour including social disinhibition, loss of initiative and interest, inability to solve problems with loss of abstract thought and impaired concentration and attention without intellectual or memory decline. This usually occurs with bilateral lesions resulting from head injury, small vessel disease, frontal degenerations e.g. frontotemporal dementias and acute hydrocephalus

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3
Q

What is the role of the cortical micturition centre in the frontal lobe? What are the symptoms of a lesion in this area?

A

this region lies in the paracentral lobule and is involved in the cortical inhibition of voiding of the bladder and bowel

incontinence

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4
Q

What is the blood supply to the frontal lobe?

A

anterior cerebral artery–supplies medial surface of the primary motor cortex, which controls the leg

medial cerebral artery–supplies lateral surface of primary motor cortex which controls face and arm

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5
Q

What is hemiplegia and monoplegia?

A

Monoplegia refers to weakness of one limb (either arm or leg) and hemiplegia refers to weakness of one arm and leg on the same side of body (either left or right side)

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6
Q

Focal seizures arising from the frontal cortex give what presentation?

A

clonic movements of the contralateral lower face, arm and leg and conjugate deviation of the head and eyes away from convulsing side (i.e. away from side of lesion)

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7
Q

What is the function of the primary somatosensory cortex in the parietal lobe?

A

located in the postcentral gyrus
PERCEIVES complex somatosensory stimuli from contralateral side of face and body
it received afferent projections via the thalamus from the somatosensory pathway
the fibres are represented in a homonculus, similar to that of the primary motor cortex

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8
Q

What is the role of the language centre in the parietal lobe?

A

found in dominant hemisphere
pathways within the arcuate fasiculus connect Broca’s area (frontal lobe) with Wernicke’s area (posterior temporal) pass through the inferior parietal region

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9
Q

What is the role of the ‘body awareness’ area in the parietal lobe?

A

integration of somatosensory, visual and auditory information (mainly non-dominant)–allows awareness of the body and its surroundings, appropriate movement of the body and constructional ability

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10
Q

What are the functions of the parietal lobe?

A

Somatosensory perception and integration of visual and somatospatial information

interpreting information such as touch, taste, temperature, visual-spatial processing, identifies where body parts are in relation to each other

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11
Q

Give some symptoms of a parietal lobe lesion

A

discriminative sensory impairment of the opposite side of the face and limbs–impairment of joint position sense. Pain, temp, vibration and touch are intact
visual disturbance

dominant lobe–
Wernicke’s dysphasia (speech is fluent but words are replaced with partly correct words and incorrect words related to word intended- paraphasia)
Gerstmann’s syndrome–inability to differentiate L and R sides of body
bileteral ideomotor and ideational apraxia

constructional apraxia, dressing apraxia, contralateral sensory inattention

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12
Q

Focal seizures of the parietal lobe may manifest as what symptoms?

A

sensory symptoms on contralateral side of body e.g. pins and needles
dyslexia, dyscalculia
apraxia–inability to carry out complex tasks despite having an intact sensory and motor system

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13
Q

What is the blood supply to the parietal lobe?

A

middle cerebral artery

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14
Q

What are the functions of the temporal lobe?

A

Wernicke’s area in dominant hemisphere–comprehension of written and spoken language

auditory and vestibular cortices
limbic system
limbic system–olfactory and taste centre. Memory, learning and emotion

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15
Q

What are symptoms of lesion in temporal lobe?

A

Wernicke’s area–receptive dysphasia
auditory agnosia–inability to recognise sounds
vestibular dysfunction
olfactory and taste hallucinations
learning difficulties
memory impairment
emotional disturbances

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16
Q

What is the function of the occipital lobe? What symptoms of a lesion in this area?

A

pereception of vision
contralateral homonymous hemianopia–central vision intact with loss of peripheral vision
cortical blindness
visual agnosia–impairment of recognising faces and objects

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17
Q

What are the structures of the basal ganglia?

A

The basal ganglia are a group of structures found deep within the cerebral hemispheres. The structures generally included in the basal ganglia are the caudate, putamen, and globus pallidus in the cerebrum, the substantia nigra in the midbrain, and the subthalamic nucleus in the diencephalon. Despite the name, the basal ganglia are not actually ganglia

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18
Q

What is the function of the basal ganglia?

A

The basal ganglia receive information from the cortex, much of which is sent first to the caudate and putamen (which together are often referred to as the striatum). After the information is processed by the basal ganglia, it is sent back to the cortex by way of the thalamus.
The functions of the basal ganglia in motor control are to facilitate movement and inhibit competing movements. For example, when someone tries to make an intentional movement like reaching for a pencil, the basal ganglia help to facilitate the movement by allowing motor plans associated with that movement (reaching and grasping in this case) to be activated. At the same time, the basal ganglia cause motor plans that might counteract the movement (perhaps flexing in this case) to be inhibited. The result is a smooth and fluid movemen

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19
Q

What are the components of the diencephalon?

A

The diencephalon is a small part of the brain that is mostly hidden from view when you are looking at the outside of the brain. It is divided into four parts: the epithalamus, thalamus, subthalamus, and hypothalamus. The diencephalon can be found just above the brainstem between the cerebral hemispheres; it forms the walls of the third ventricle. The only part of the diencephalon that can be seen without taking a cross-section of the brain is the bottom-most portion of the hypothalamus.

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20
Q

What is the role of the epithalamus?

A

The epithalamus consists primarily of the pineal gland and the habenulae. The pineal gland is an endocrine gland that secretes the hormone melatonin, which is thought to play an important role in the regulation of circadian rhythms.

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21
Q

What is the role of the subthalamus?

A

portion of the subthalamus is made up of tissue from the midbrain extending into the diencephalon. Thus, parts of midbrain regions like the substantia nigra and red nucleus are found in the diencephalon. The subthalamus is also home to the subthalamic nucleus and the zona incerta. The subthalamic nucleus is densely interconnected with the basal ganglia, and plays a role in modulating movement. The zona incerta has many connections throughout the cortex and spinal cord, but its function is still not determined. Several collections of important fibers (e.g. somatosensory fibers) also pass through the subthalamus.

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22
Q

What is the role of the thalamus?

A

two oval collections of nuclei - make most of the mass of diencephalon.

relay station = almost all sensory information (exception of smell) that proceeds to the cortex first stops in the thalamus before being sent on to its destination.

The structure is subdivided into a number of nuclei that possess functional specializations for dealing with particular types of information. Sensory information thus travels to the thalamus and is routed to a nucleus tailored to dealing with that type of sensory data. Then, the information is sent from that nucleus to the appropriate area in the cortex where it is further processed.

The thalamus doesn’t deal just with sensory information, however. It also receives a great deal of information from the cerebral cortex, and it is involved with processing that information and sending it back to other areas of the brain. Due to its involvement in these complex networks, the thalamus plays a role in a number of important functions ranging from sleep to consciousness.

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23
Q

Clusters of axons in the PNS and CNS are called what?

A

nerves in PNS
tracts in CNS

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24
Q

What cells are responsible for myelination of axons?

A

oligodendrocytes in CNS
Schwann cells in PNS

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25
Q

Name the CNS glial cells

A

ASTROCYTES: structural and metabolic support for neurons. Most abundant. Determine capillary permeability of blood brain barrier. Control chemical movement

  • *MICROGLIAL CELLS-**-phagocytosis
  • *OLIGODENDROCYTES-**-forms myelin sheath
  • *EPENDYMAL CELLS**–line cavities of brain and spinal cord, cilia assist in CSF circulation. Form partially permeable barrier between CSF
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26
Q

What are the roles of astrocytes,

A

CNS glial cells
astrocytes–structural and metabolic support for neurons. Most abundant. Determine capillary permeability of blood brain barrier. Control chemical movement

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27
Q

What are the roles of microglial cells?

A

microglial cells–phagocytosis

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28
Q

What are the roles of oligodendrocytes

A

oligodendrocytes–forms myelin sheath

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29
Q

What are the roles of ependymal cells?

A

ependymal cells–line cavities of brain and spinal cord, cilia assist in CSF circulation. Form partially permeable barrier between CSF

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30
Q

What are the glial cells of the PNS system?

A
  • *satellite cells–**similar to astrocytes, metabolic and structural support for neurons
  • *schwann cells-**-form myelin sheath
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31
Q

What are the roles of the ventral, dorsal and lateral horns of the spinal cord?

A

ventral–receive info from brains motor cortex, sends it to skeletal muscles to trigger voluntary movement

dorsal–take sensor info and send to brains sensory cortex

lateral–help regulate processes like urination, digestion, HR. Mostly SNS activity

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32
Q

What are the roles of the parts of the brainstem?

A

basic life sustaining functions e.g. breathing, BP

midbrain– vision, hearing, motor control, sleep wake cycle, consciousness
pons–facial expressions and sensations, body equilbrium, posture
medulla–respiratory centre, swallow, cough, vomit, BP

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33
Q

In the SNS, where are the preganglioninc and postganglionic neurons located?

A

preganglioninc neurons located in thoracolumbar spinal cord’s intermediate horn (T1-L2). Release ACh

postganglionic neurons–located close to spinal cord.
Paravertebral ganglia (cervical, thoracic, lumbar, pelvic)
Prevertebral (cerlial, superior mesenteric, inferior mesenteric)
Most are adrenergic but some release ACh

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34
Q

In SNS, what type of neurotransmitters are released?

A

preganglioninc neurons release ACh which bind to nicotinic receptors on post-ganglionic neurons

postganglioninc neurons are usually adrenergic (noradrenaline)
but some are cholinergic but ACh binds to muscarininc, NOT nicotinic receptors on organs

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35
Q

In the PNS, where are the preganglioninc and postganglionic neurons located?

A

preganglionic–located in brainstem (nuclei of CN III, VII, IX and X) and sacral spinal cord (S2-4)
they release ACh which binds to nicotinic receptors on postganglionic cell bodies

postganglionic neurons are located close to target organs/in target organs.
mostly cholinergic but some release neuropeptides. Effector receptors are muscarinic

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36
Q

What are the terminal branches of the brachial plexus?

A

MARMU
musculocutaneous
axillary
radial
musculocutaneous
ulnar

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37
Q

What are the roots of the brachial plexus?

A

C5, C6, C7, C8, T1

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38
Q

How many cranial nerves originate from the midbrain and above, the pons and the medulla?

A

3 groups of 4
4 from midbrain and above
4 from pons
4 from medulla
remember, a lesion on the brainstem will usually produce ipsilateral cranial nerve defects

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39
Q

What cells keep CSF in motion?

A

cilia of ependymal cells lining ventricular system

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40
Q

Where is CSF produced?

A

mostly (80%) by choroid plexus–network of capillaries, modified ependymal cells in ventricles
remaining 20% is made by ependymal cells lining subarachnoid space

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41
Q

CSF leaves the 4th ventricle by way of the…

A

3 apertures
R aperture of luschka

L aperture of luschka
median aperture of magendie

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42
Q

What is the rbc, WBC, protein and glucose content of CSF?

A

no rbc
wbc <5/ml
protein <0.5mg/ml
glucose 60-70% of blood levels (2.5-5mmol)

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43
Q

What is a normal opening pressure in a lumbar puncture?

A

<20cm in water is normal
21-29 intermediate
>30 is high
remember you cannot estimate pressure if patient is sitting up for LP

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44
Q

What are the causes of hydrocephalus?

A

CSF accumulation in brain–>increased ICP
symptoms: headaches, double vision, poor balance, mental impairment and increased head size in kids, vomiting, sleepy, seizure, downward pointing eyes

causes: birth defects (neural tube, aqueductal stenosis) or acquired.
Meningitis, brain tumour, traumatic head injury, intraventricula hemorrhage and subarachnoid haemorrhage

treat using a shunt

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45
Q

What are the symptoms of idiopathic intracranial hypertension?

A

Increased intracranial pressure in the absence of a tumor or other etiology seen on imaging.

Symptoms: headache, pulsatile tinnitus, diplopia, papilloedema (risk of blindness), mydriasis (dilated pupils)

more common in young, overweight women, may be associated with cerebral venous sinus thrombosis

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46
Q

What is the treatment of idiopathic intracranial hypertension?

A

weight loss
repeated lumbar puncture
shunt
acetazolamide–diuretic used to treat altitude sickness

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47
Q

What is a papilloedema?

A

Optic disc swelling that is caused by increased intracranial pressure due to any cause. The swelling is usually bilateral and can occur over a period of hours to weeks. Unilateral presentation is extremely rare.

In intracranial hypertension, the optic disc swelling most commonly occurs bilaterally. When papilledema is found on fundoscopy, further evaluation is warranted because vision loss can result if the underlying condition is not treated. Further evaluation with a CT or MRI of the brain and/or spine is usually performed.

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48
Q

What is brain herniation

A

brain tissue displacement through the skull opening or dural fold due to increased intracranial pressure

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49
Q

What is Cushing’s triad?

A

hypertension
bradycardia
irregular respirations

physiological nervous system response to increased intracranial pressure (ICP) that results in Cushing’s triad of increased blood pressure, irregular breathing, and bradycardia. It is usually seen in the terminal stages of acute head injury and may indicate imminent brain herniation. It can also be seen after the intravenous administration of epinephrine and similar drugs

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50
Q

Differentiate between encephalitis and meningitis?

A

meningitis–inflammation of the meninges of the brain (leptomeninges–pia and arachnoid)

encephalitis–inflammation of the brain
can occur together = meningoencephalitis

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51
Q

What are the symptoms/signs of meningitis?

A

fever, nausea, vomiting, lethargy, irritable, anorexia, headache, muscle/joint ache, respiratory symptoms (cough)
stiff neck, altered mental state, non-blanching rash, bulging fontanelle (infants), photophobia, kernig’s sign, brudzinski sign
coma, paresis, focal neurological deficit, seizure

ask about: recent exposure, recent infection, IV drug use, head trauma, HIV, immunocompromising conditions

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52
Q

What is Bruzinski’s sign?

A

flexion of the neck with the child supine causes flexion of knees and hips
meningitis

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53
Q

What is kernig’s sign?

A

After flexing the hip and knee at 90 degree angles, pain and resistance are noted.

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54
Q

What is opisthotonus?

A

Sustained contraction of the back muscles resulting in arched position

late sign of meningeal irritation and raised ICP

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55
Q

What WBC are found in bacterial meningitis?

A

neutrophils
all other causes give lymphocytes

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56
Q

What effect does meningitis infection have on WBC, blood glucose, protein and ICP?

A

WBC increase (higher in viral causes)
glucose decreases to <2/3 of blood level
pressure increases
protein increases >50mg/dl

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57
Q

What are the causative microorganisms of meningitis by age group

A

Explaining Big Hot Neck Stiffness
infants: E.coli, group B streptococcurs
kids: Haemophilus infleunzae
young adult: Neisseria meningitidis
elderly: Streptococcus pneumoniae

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58
Q

What is the empirical treatment for bacterial meningitis?

A

cefotaxime or ceftriaxone
dexamethasone
if patient over 55 add in ampicillin or amoxicillin

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59
Q

What is the treatment for meningococcal meningitis?

A

benzylpenicillin
or cefotaxime or ceftriaxone
or chloramphenicol if allergic to beta lactams
PLUS dexamethasone

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60
Q

What is a brain abscess?

A

Brain abscess is an abscess caused by inflammation and collection of infected material, coming from local (ear infection, dental abscess, infection of paranasal sinuses, infection of the mastoid air cells of the temporal bone, epidural abscess) or remote (lung, heart, kidney etc.) infectious sources, within the brain tissue. The infection may also be introduced through a skull fracture following a head trauma or surgical procedures.

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61
Q

What is the treatment for a brain abscess?

A

drainage
plus cefotaxine or ceftriaxone

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62
Q

What are symptoms of brain abscesses?

A

fever, progressively worsening focal neurology, headache, raised ICP while supine, morning vomiting, mental status change, seizure, papilloedema

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63
Q

Differentiate between encephalopathy and encephalitis?

A

encephalopathy–clinical syndrome of altered mental status manifesting as reduced consciousness, altered consciousness, altered cognition/personality/behaviour
has many causes: infection, metabolic derrangement, trauma etc

encephalitis is inflammation of the brain

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64
Q

List the most common causative organisms of encephalitis

A

HSV-1 most common
HSV-2
epstein barr, influenza

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65
Q

What is acyclovir?

A

Aciclovir, also known as acyclovir, is an antiviral medication. It is primarily used for the treatment of herpes simplex virus infections, chickenpox, and shingles.

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66
Q

What is treatment of tension headache according to NICE guidelines

A

analgesia (NOT opioids)
if consistent or chronic: Pharmacological prophylaxis with low dose amitriptyline (10-75mg daily)For people who do respond — attempt withdrawal of medication if improvement is maintained for 4-6 months. Withdraw if no response
advise about anelgesia overuse

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67
Q

What is treatment of migraine according to NICE?

A

keep diary–look for triggers
Ensure that women who have migraine with aura are not using combined hormonal contraception, as this is contraindicated.
restrict analgesia to 2 days a week

offer a triptan
sumatriptan
and an antiemetic metoclopramide 10mg or prochlorperazine 10mg

prophlaxis: beta blocker, amitriptyline

What are triptans?

selective serotonin (5-HT1) agonist ex: sumatriptan

structurally similar to serotonin, reduce vascular inflammation, constrict blood vessels. Used in migraine treatment

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68
Q

What are trigeminal autonomic cephalgias?

A

Trigeminal autonomic cephalalgia (TAC) is the name for a type of primary headache that occurs with pain on one side of the head in the trigeminal nerve area and symptoms in autonomic systems on the same side, such as eye watering and redness or drooping eyelids.
Cluster headache most common type
recurrent pain in trigeminal distribution with autonomic features (eye watering, nasal congesion, red eye)

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69
Q

What is a cluster headache?

A

severe, unilateral, retro-orbital headache with restlessness, agitation, ipsilateral lacrimation, rhinorrhoea
short lived 15-90 mins but occur frequently and repeatedly (same time each day) in clusters lasting days to weeks
months without symptoms
males more commonly

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70
Q

What is the treatment of a cluster headache?

A

triptans, oxygen
high dose verapamil (Ca2+ block, up to 960mg/day)

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71
Q

What is a subarachnoid haemorrhage?

A

bleeding into the subarachnoid space
symptoms: thunderclap headache, vomit, decreased level of consciousness, fever, and sometimes seizures. Neck stiffness or neck pain are also relatively common.

SAH may occur as a result of a head injury or spontaneously, usually from a ruptured cerebral aneurysm.Risk factors for spontaneous cases included high blood pressure, smoking, family history, alcoholism, and cocaine use. Generally, the diagnosis can be determined by a CT scan of the head if done within six hours of symptom onset.

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72
Q

What is cerebral venous sinus thrombosis?

A

presence of a blood clot in the dural venous sinuses, which drain blood from the brain. Symptoms may include headache, abnormal vision, any of the symptoms of stroke such as weakness of the face and limbs on one side of the body, and seizures.
symptoms: thunderclap headachea
often in female patients on oral contraceptive pill
MRI scan

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73
Q

What is temporal arteritis?

A

AKA giant cell arteritis due to subacute granulomatous inflammation of the large vessels
closely associated with polymyalgia rheumatica (aches in shoulder, neck and pelvis)
rare <50 years
localised headache
jaw claudication
visual loss
tender temporal arteries
visual loss
urgent treatment with steroids due to risk of blindness

How well did you know this?
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74
Q

What is the likely cause of headaches in obese patient that snores with COPD?

A

sleep apnoea with CO2 retention

75
Q

What is glioblastoma multiforme?

A

Glioblastoma, also known as glioblastoma multiforme (GBM), is the most aggressive cancer that begins within the brain. Initially, signs and symptoms of glioblastoma are non-specific. They may include headaches, personality changes, nausea, and symptoms similar to those of a stroke.

[1] Worsening of symptoms often is rapid. This may progress to unconsciousnes

76
Q

What are alpha, beta, theta and delta brain waves?

A

alpha–low amplitude, regular, rhythmic. Appear during relaxed consciousness
beta–rhythmic but increased frequency and decreased regularity compared to alpha. Appear during alert consciousness states.
theta–irregular
delta–increased amplitude, often during deep sleep and anesthesia. in awake adults may indicate brain damage

77
Q

What are the stages of sleep?

A
  1. immediately after falling asleep
  2. first 30-45 mins, theta wave present
    3/4 slow wave sleep, 90 mins into sleep.

REM–rapid eye movement sleep–characterised by alpha waves (typically seen when awake), increased HR, BP RR, increased O2 use, most dreaming occurs here, memory consolidation

78
Q

What is the reticular formation?

A

diffuse collection of networks of neurons spanning all 3 divisions of brainstem
NT include noradrenaline, serotonin, ACh therefore has diverse functions

it projects to thalamus, hypothalamus, some brainstem nuclei, cerebellum, spinal cord and cerebral cortex
receives input from sensory systems

79
Q

What neurons are normally active during wakefulness?

A

orexingeric–found in lateral hypothalamus
these neurons project to cerebra, arousal nuclei and ventrolateral preoptic nucleus in anterior hypothalamus, VLPO

80
Q

What is the centre for non REM sleep promotion?

A

ventrolateral preoptic nucleus in anterior hypothalamus, VLPO
it has inhibitory projections to all main arousal centres and is active during sleep
lesions to this cause insomnia

81
Q

What is the pathophysiology of narcolepsy?

A

onset is due to specific loss of orexin containing neurons in lateral hypothalamus
inherited autoimmune condition
1. repeatedly fall asleep during the day regardless of current activity
2. limb weakness during emotional episodes
3. night time or morning wakening accompanied by muscle paralysis
4. vivid dream recollection

82
Q

List the treatments for narcolepsy

A

modafanil
amphetamines
methylphenidate (Ritalin)
sodium oxybate (GHB)

83
Q

Differentiate between simple partial and complex partial seizures

A

partial–seizure begins focally

simple partial–focal with minimal spread of abnormal discharge. Normal consciousness maintained.
May have: motor symptoms, somatosensory symptoms, autonomic symptoms, psychological e.g. dejavu

complex partial–begins as simple partial then spreads. Impaired consciousness. Clinical manifestations vary with site of origin and degree of spread.

84
Q

What is a generalised seizure?

A

both hemispheres affected
can being as a partial seizure that spreads = secondarily generalised seizure
manifestations are determined by the cortical site at which the seizure arises

85
Q

What are absence seizures?

A

type of generalised seizure
‘petit mal’
sudden onset and abrupt cessation, brief duration
consciousness is altered
may have mild clonic jerking of the eyelids or extremities, postural tone changes, autonomic phenomena

onset age 4-12, attacks several times a day with duration of 5-15 seconds. Patient stares vacantly. There may be eye blinking.

86
Q

List the different types of generalised seizure

A

consciousness lost even for brief period of time
absence seizure–space out
myoclonic–short muscle twitch
clonic–convulsing
atonic–floppy
tonic-clonic–stiff then convulse
tonic–stiff, flexed

87
Q

What is a tonic-clonic seizure?

A

grand mal
sudden onset with loss of consciousness and fall to the ground. Followed by tonic phase which lasts 10 secs where body becomes stiff. Breathing stops and person may become cyanotic.
Then clonic phase which lasts 1-2 mins, violent rhythmical shaking. Eyes roll back, tongue biting and maybe loss of bladder and bowels. Breathing recommences.
Awakes with confusion with headache, myalgia and some retrograde amnesia.

88
Q

What is Lamotrigine?

A

anticonvulsant
used in epilepsy
inhibits sodium channels (prevents EPSP)
side effects: hypersensitivity

89
Q

What is sodium valproate?

A

anticonvulsant
mechanism not clear
increases GABA
side effects: hair loss, teratogenic (avoid in pregnancy), liver damage

90
Q

What is carbamazepine?

A

anticonvulsant
derivative of TCA
effective in partial seizures and trigeminal neuralgia
side effects: sedation, atraxia, mental disturbances, water retention

91
Q

What is oxcarbazepine?

A

anticonvulsant
related to carbamazepine
may augment K+ channels

92
Q

What is phenytoin?

A

anticonvulsant
block Na+ channels
not effective in absence seizures
side effect: confusion, gum hyperplasia, rashes, anemia, teratogenic, osteoporosis
sometimes used as an antidysrhythmic

93
Q

What is first line for status epilepticus?

A

IV benzodiazepine (lorazapam, diazepam)

94
Q

What imaging should be done in person with first time epilepsy?

A

MRI

95
Q

What is anosmia and hyposmia?

A

anosmia–loss of olfaction
hyposmia–reduced sense of smell
e.g. common cold, smoking, sinusitis, URTI nasal polyp

96
Q

What is ptosis?

A

drooping eyelid

97
Q

What is anisocoria?

A

unequal pupil size

98
Q

What is Horner’s syndrome?

A

Injury to the cervical sympathetic chain. Think MAP:
Miosis (small pupil)
Anhidrosis of ipsilateral face
Ptosis

causes: demyelination, neck trauma/surgery, apical lung tumour

99
Q

What is myotonic Adies pupil?

A

affected pupil dilated and unresponsive to light, constricts very slow to near vision
benign

100
Q

what is the Argyll Robertson pupil?

A

classic sign of neurosyphillis but can be seen with diabetes and severe optic nerve disease
pupil small and irregular, reacts to accommodation but not light

101
Q

What are clinical sign of occulomotor nerve palsy?

A

ptosis–droop eyelid
eye deviated laterally and downwards, pupil may be dilated and unresponsive

102
Q

What are signs of trochlear nerve palsy?

A

impaired depression of fully adducted eye, head may be tilted to opposite side to avoid diplopia when reading or looking down to walk downstairs

103
Q

What are signs of abducens nerve palsy?

A

impaired abduction

104
Q

Differentiate between sensorineural and conductive hearing loss

A

sensorineural–something wrong with auditory nerve of the cochlea
conductive–problem with sound passing to inner ear

105
Q

In Weber’s test, if the sound is louder on the right side what does this mean?

A

either
1. conductive loss in R ear
or
2. sensorineural loss in L ear

then go on to do rinne’s test
if rinne’s test is positive (louder on mastoid process) then there is right sided conductive hearing loss

106
Q

What is the motor cortex? What are the subdivisions?

A

region in cerebral cortex dedicated to voluntary movement planning, control and execution
location: posterior precentral gyrus in frontal lobe
divided into regions:
1. primary motor cortex–arranged into motor homonculus. Located just anterior to central sulcus
2. non-primary motor cortex–located anterior to primary motor cortex. The non primary motor cortex is composed of the pre-motor cortex (movement preparation) and the supplementary motor cortex (movement planning sequences and preparation)

107
Q

What are alpha motor neurons?

A

lower motor neurons

108
Q

What is the difference between pyramidal and extra pyramidal tracts?

A

Pyramidal–UMN synapse with LMN in anterior horn of spinal cord. Pyramidal tracts include corticospinal and corticobulbar tract. These are aggregations of efferent nerve fibers from the upper motor neurons that travel from the cerebral cortex and terminate either in the brainstem (corticobulbar) or spinal cord (corticospinal) and are involved in the control of motor functions of the body.

Extrapyramidal–Extrapyramidal tracts are chiefly found in the reticular formation of the pons and medulla, and target lower motor neurons in the spinal cord that are involved in reflexes, locomotion, complex movements, and postural control.

109
Q

Explain the pathway of the corticospinal tract

A

Cell bodies of UMN located in motor cortex. The axons of these fibres travel to brainstem where they form medullary pyramids on ventral surface of the brainstem.
At the medullary pyramid, 90% of the corticospinal tract fibres decussate to form the lateral corticospinal tract. This is responsible for the fine motor movement of upper and lower limbs.

10% of the fibres form the anterior corticospinal tract. They do not decussate at the medullary pyramids. They eventually decussate at the spinal level they innervate. Responsible for gross, postural movement of the trunk.

110
Q

What is the difference between the anterior and lateral corticospinal tracts?

A

Cell bodies of UMN located in motor cortex. The axons of these fibres travel to brainstem where they form medullary pyramids on ventral surface of the brainstem.
At the medullary pyramid, 90% of the corticospinal tract fibres decussate to form the lateral corticospinal tract. This is responsible for the fine motor movement of upper and lower limbs.

10% of the fibres form the anterior corticospinal tract. They do not decussate at the medullary pyramids. They eventually decussate at the spinal level they innervate. Responsible for gross, postural movement of the trunk.

111
Q

Explain the pathway of the corticobulbar tract

A

Cell bodies of UMN located in the motor cortex. These axons travel lateral to the corticospinal tract and reach the brainstem.

The fibres decussate at the cranial nerve level they synapse with. Therefore, they cross and cranial nerve LMN that receive UMN branches are CN V, VII, XI, XII.
Some of the UMN synapse with BOTH the contralateral AND ipsilateral CN nuclei of CN V, XI, and part of VII that supplies upper half of face.

Therefore, these muscles receive signals from both hemispheres of the brain.

112
Q

Where do extrapyramidal tracts originate?

A

They do not start in the cerebral cortex.
Instead, the UMN are located in the brainstem.

Controls reflexes, locomotion, complex movements and posture. Modulated by nigrostriatal pathway, basal ganglia, cerebellum, vestibular nuclei, sensory areas of cerebral cortex.

damage to extrapyramidal tracts–various types of dyskinesias (involuntary movement disorders)

113
Q

What are the functions of the cerebellum?

A

coordinating movement, control posture, balance, fine motor movement and motor learning

114
Q

How is the cerebellum connected to the brainstem?

A

3 sets of cerebellar peduncles: superior, middle, inferior

115
Q

What separates the 2 hemispheres of the cerebellum?

A

vermis

116
Q

Name the 3 lobes of the cerebellum?

A

anterior lobe

posterior lobe

flocculonodular lobe

117
Q

Name the 3 layers of the cortex of the cerebellum?

A

from outer to inner

  1. molecular layer–various neurons synapse with each other
  2. purkinje layer–cell bodies of purkinje fibres
  3. granular layer–cell bodies of granular cells
118
Q

input from the cerebrum and spinal cord comes into the cerebllum from which 2 types of axons?

A

mossy fibres and climbing fibres

119
Q

What are the functions of the 3 lobes of the cerebellum?

A

anterior–the small anterior lobe and the anterior superior vermis (spinocerebellum) are involved in receiving proprioceptive info from limbs

posterior–the large posterior lobe and middle part of vermis (neocerebellum) are involved in receiving inputs from contralateral cerebral cortex via pontine nuclei. It is involved in fine motor control e.g. finger movement

floconodular lobe (vestibulocerebellum)–and inferior vermis together involved in controlling info from vestibular system

120
Q

List clinical features of cerebellar dysfunction

A
  • *ataxia** of limbs and gait
  • *dysarthria** - motor speech disorder
  • *nystagmus** - irregular eye motion
  • *dysdiadochokinesis -** inability perform rapid, alternating movements

cerebellar dysfunction causes impairment of the process of controlling movements once they have been initiated. This gives rise to ataxia.

Ataxia is a term for a group of disorders that affect co-ordination, balance and speech

121
Q

What is ataxia?

A

Ataxia is a neurological sign consisting of lack of voluntary coordination of muscle movements that can include gait abnormality, speech changes, and abnormalities in eye movements. Ataxia is a clinical manifestation indicating dysfunction of the parts of the nervous system that coordinate movement, such as the cerebellum

Gait–wide based staggering gait.
Dysarthric speech–slow, slurred
Abnormal eye movements–nystagmus

122
Q

In unilateral cerebellar hemisphere lesion, unsteadiness is to what side?

A

side of the lesion

123
Q

What is titubation?

A

nodding tremor of head in A-P plane, sometimes seen in cerebellar disorders

124
Q

List some causes of cerebellar dysfunction

A

tumour, abscess
MS
vascular, infarction
infection, encephalitis
toxins, anticonvulsants, alcohol
inherited (friedreich ataxia)

125
Q

What are the basal ganglia?

A

symmetrical groups of grey matter or nuclei deep within the cerebral hemispheres and brainstem.
The main components are the caudate nucleus, globus pallidus, putamen, substantia nigra and subthalamus.
These nuclei are involved with controlling movement, especially the initiation and termination of movement. For smooth movement.
Influence motor cortex via pathways through the thalamus.

126
Q

Disease of the basal ganglia leads to what?

A

leads to extrapyramidal disorders of movement, including tremor
chorea–rapid, irregular, jerky movement affecting face, trunk, limbs
athetosis, dystonia, akathisia and tics

127
Q

What is a resting tremor typical of?

A

most common cause is parkinsons (pill rolling tremor) at rest and can improve with movement

128
Q

What is a physiological tremor?

A

affects all muscle groups, but most commonly noted in hands
causes: alcohol withdrawl, drugs (lithium, sodium valproate), tea and coffee

129
Q

What is an essential tremor?

A

hard to distinguish from physiological tremor but is slower and coarser
involves head and upper limbs but spares lower limb
can be inherited
can be disabling

130
Q

What tremor is associated with cerebellar dysfunction?

A

intention tremor
absent at rest and becomes apparent on movement

131
Q

What is tardive dyskinesia? What causes it?

A

often irreversible movement disorder which can include chorea, dysphonia, tics and myoclonus
caused by some antipsychotic drugs

132
Q

What are the 3 classifications of somatosensory fibres?

A

non-myelinated fibres–(type C) slowest, sense burning pain, hot temperature
small myelinated fibres–(Adelta) faster, sense sharp pain, gross touch and cold temp
large myelinated–Aalpha, Abeta, fastest, sense proprioception, vibration and fine touch

133
Q

The somatosensory pathways are made up of relays of how many neurons?

A

4
1st order neuron–has sensory receptors, converts stimuli into impulse
2nd order–cell body in spinal cord or brainstem, synapse with 3rd order
3rd order–cell body in thalamus, sends signal to somatosensory cortex
4th order–cell body in sensory cortex

134
Q

What senses do the medial leminiscal pathway conduct info about?

A

fine touch, proprioception
with large myelinated fibres

135
Q

Describe the medial leminiscal pathway

A

fine touch, proprioception
with large myelinated fibres

large myelinated fibres of 1st order neurons run to spinal cord and through the dorsal horn.
1st order neurons synapse in the medulla
2nd order neurons run to medial lemniscus and decussates in medial leminscus, runs through the pons, midbrain to the thalamus
3rd order neurons synapse in thalamus
3rd order neurons run to sensory cortex in parietal lobe
4th order neurons synapse in sensory cortex

136
Q

What senses do the spinothalamic pathway conduct info about?

A

pain, temperature and crude touch
small myelinated fibres (Adelta)–sharp pain and cold temperature
non-myelinated fibres–type C–burning pain, hot temperature, crude touch

137
Q

Outline the spinothalamic tract

A

pain, temperature and crude touch
small myelinated fibres (Adelta)–sharp pain and cold temperature
non-myelinated fibres–type C–burning pain, hot temperature, crude touch

1st order neurons synapse in posterior horn of spinal cord.
Small myelinated fibres A delta enter through dorsal root and travel up 2 vertebral segments.
Non-myelinated C fibres follow the same pathway but synapse with interneurons first i.e. before reaching the posterior horn

2nd order neurons decussate and cross to anterior horn of spinal cord
neurons carried through one of 2 tracts to the thalamus
lateral tract–pain temp, pressure
anterior tract–crude touch
synapse with 3rd order in thalamus, then 3rd order go to somatosensory cortex in parietal lobe, 4th order synapse in sensory cortex

138
Q

What fluids are contained within the bony and membranous labyrinth?

A

perilymph in bony
and endolymph in membranous

139
Q

What do the saccule and utricle do?

A

2 otolith containing organs they sense gravity and linear acceleration (static equilbrium)

saccule–monitors verticle movement S for SKY
utricle monitors horizontal movement
contain endolymph

140
Q

What are macula? Describe how it works

A

hair cells found within the utricle and saccule
they have sterocilia and a long kinocilia
these hair cells are embeded in an otolithic membrane and otoconia are calcium carbonate stones that sit on top of the jelly membrane

the movement of otolithic membrane bends the cilia and kinocilium in a specific way
tip link on the shorter stereocilia opens K+ channel on longer stereocilia and K+ flows into hair cell and causing depolarisation
depolarisation opens voltage gated Ca2+ channels and ESPS sent up to brain

141
Q

What is the function of the semicircular canals?

A

monitor rotational acceleration and deceleration
three planes of orientation and within each canal is a semicircular duct, within the duct is an ampulla
in the ampulla there is hair cells (but no otoliths), movement of endolymph causes movement of cupula

bending towards kinocilium causes depolarisation and increased AP’s

142
Q

What is physiologic nystagmus?

A

Physiological nystagmus is a form of involuntary eye movement that is part of the vestibulo-ocular reflex (VOR), characterized by alternating smooth pursuit in one direction and saccadic movement in the other direction.

  1. slow phase–smooth movement of eyes in opposite direction
  2. fast phase–eyes quickly jump back in same direction of movement

direction of the fast phase defines the nystagmus

143
Q

What is the coloric reflex test?

A

tests condition of brainstem
put warm water in ear causes nystagmus to same side
cold water causes nystagmus to opposite side
COWS
in braindead patients, there is no fast nystagmus, only slow component

144
Q

Name the 4 deep cerebellar nuclei

A

lateral to medial
Dont Eat Greasy Food
dentate nucleus
emboliform nucleus
globose nucleus
fastigial nucleus

145
Q

What is meniere’s disease and give the symptoms

A

idiopathic inner ear disorder, recurrent attacks of vertigo and progressive hearing loss
tinnitus, sense of ear fullness due to excess endolymph fluid in inner ear

symptoms: spontaneous vertigo (20 mins-24 hrs) fatigue, nausea, vomitting, ear fullness, tinnitus, progressive hearing loss
treatment: beta histine, surgical decompression, antihistamines, antiemetic, anticholinergic

146
Q

What is labyrinthitis?

A

inflammation of the inner ear (vastibular neuritis) and when it progresses to unilateral hearing loss it is called labyrinthitis

causes: viral, bacterial, head injury, allergy, stress, URTI
symptoms: severe vertigo, fatigue, nausea, vomiting, nystagmus, tinnitus, heading loss,

147
Q

What are the red flag features in dizziness?

A

any of the following raises suspicion of serious intracranial pathology
if presentation is acute consider stroke, when less acute consider SOL and refer for CT
focal neurological symptoms: dysarthria, diplopia, facial weakness, swallow difficulties, dysdiadokinesis, focal limb weakness

papilloedema, drowsy
atypical nystagmus
new onset headache
progressive unilateral hearing loss (refer to MRI to exclude acoustic neuroma)

148
Q

What is the difference between peripheral and central vertigo?

A

peripheral–damage to vestibular apparatus or to the vestibular nerve. Causes–BPPV, vestibular neuritis, Menieres disease, acoustic neuroma

central–damage to vestibular structures in the brain stem or cerebellum. Causes–posterior circulation stroke, brain tumour, migraine, MS

149
Q

What are the differences in the nytagmus between central and peripheral causes of vertigo?

A

in central nystagmus can be horizontal, torsional, rotary and vertical. Usually no lag time between dix hallpike and onset. Nystagmus usually lasts more than one minute.

peripheral–never vertical. 2-40 second lag time between manoeuver and onset. Nystagmus lasts less than one minute.

150
Q

What age is MS usually diagnosed? Are men and women equally affected? Where is it most common?

A

20-40
women more affected in 3:1 ratio
higher incidence at latitudes closer to the poles
European descent more commonly affected however, black Americans may have more aggressive courses due to socioeconomic reasons

151
Q

What allele has been found to be associated with MS?

A

HLADRB1–accounts for 52% of the variation in MS prevalance by latitude in Europe

152
Q

What virus are most individuals with MS infected with?

A

>99% have EBV

153
Q

What type of hypersensitivty reaction is MS?

A

type IV hypersensitvity

154
Q

Describe the pathophysiology of MS

A

autoimmune type IV hypersensitivity demyelinating disease
T cells break through BBB and get activated by myelin proteins
Cytokines produced and oligodendrocytes damaged. BBB compromised. B cells produce antibodies against myelin proteins. Oligodendrocytes engulfed.
Damage and loss of axons

155
Q

What are the symptoms of MS?

A

charcots neurologic triad–dysarthria, nystagmus, intention tremor

depends on plaque location
brainstem—conscious movements e.g. difficulty eating and unconscious movements–difficulty swallowing
eye nerves–optic neuritis e.g. loss of vision, double visiojn
motor pathwyas–muscle weakness, spasm, tremor, ataxia, paralysis
sensory pathways–numb, pins and needles, paresthesias
autonomic nervous system–constipation, urintary incontience, sexual dysfunction

156
Q

What features are seen of MRI of MS patient?

A

dawsons fingers–plaques radiating outwards from corpus callosum

157
Q

What are treatments for MS?

A

if relapse affects function then high dose methylprednisolone

in relapsing and remitting types: disease modifying therapies (include interferon beta preparations, glatiramer, dimethyl fyumarate and teriflunomide)

158
Q

What is the role of interferon beta treatment in MS?

A

interfere with formation of new demyelinating plaques in the CNS and have relapse reduction rates of 30%

159
Q

What is side effect of too much vitamin D?

A

hypercalcemia–can cause kidney and bile stones, nausea, vomiting, psychological effects and abnormal heart rhythms

160
Q

What are the signs of cerebellar dysfunction?

A

DASHING
Dysdiadochokinesis
Ataxia (Trunk, Limb dysmetria)
Scanning/staccato speech
Hypotonia (due to lack of cerebellar input)
Intention tremor
Nystagmus
Gait (wide)

161
Q

Positive Romberg’s test indicates what?

A

unsteadiness on standing with eyes open is common in cerebellar disorders.
Instability that only occurs or is markedly worse on eye closure (positive romberg’s sign) indicates sensory ataxia or bilateral vestibular failure.

This is a test of proprioception, not of cerebellar disease. Swaying with correction is not a positive result (although this may occur in cerebellar disease). Falling without correction is abnormal and indicates unsteadiness is due to a sensory ataxia from lack of proprioception, rather than a cerebellar ataxia.

162
Q

When assessing gait, if there is a unilateral cerebellar lesion where does the patient veer towards?

A

side of the lesion

163
Q

What is hemiplegic gait?

A

unilateral UMN lesion
extension at the hip, knee and ankle and circumduction at the hip such that the food on the affected side is plantar flexed and describes a semicircle as the patient walks. Upper limb is also flexed.

164
Q

An absence or and an an excessive rebound phenomenon in cerebellar examination is suggestive of what?

A

An exaggerated version of the normal response is suggestive of spasticity.

The absence of rebound phenomenon is suggestive of cerebellar disease.

165
Q

What are the consequences of not telling the DVLA about a medical condition that affects your driving?

A

fine of up to £1000 and may be prosecuted if youre involved in an accident as a result

166
Q

What are rules for epilepsy and driving? And TIA/stroke

A

6 months off after first seizure
if have epilepsy refrain for 1 year from date of attack
if antiepileptic drug is stopped or change must inform DVLA and stop driving and reapply after 6 months

TIA–1 month off
If TIAs are recurrent, need 3 months clear

167
Q

What is the cause of beriberi?

A

thiamine B1 deficiency

168
Q

What are the symptoms of beriberi?

A

cause: thamine B1 deficiency
Nystagmus, ataxia, ophthalmoplegia (triad of Wernicke-Korsakoff syndrome), confusion

Wet beriberi–tachycardia, dyspnea, edema

Dry beriberi–peripheral neuropathy, confusion, pain; AKA Wernicke-Korsakoff syndrom

169
Q

What is the cause of hepatic encephalopathy?

A

Brain injury due to toxic metabolites; not removed by liver due to liver dysfunction
Accumulation of toxic metabolites (e.g. ammonia), byproduct of nitrogen metabolism
Ammonia detoxification in astrocytes →glutamine accumulation → osmotic stress → swelling

raised ammonia in blood

170
Q

What medications treat hepatic encephalopathy?

A

lactulose–Decrease absorption of ammonia
Rifaximin–Kill bowel flora that produce ammonia

171
Q

What is Wernicke-Korsakoff syndrome?

A 
cause by thamine B1 deficiency
earlier stage--Wernicke's encephalopathy (reversible) but if untreated leads to..
Korsakoff syndrome (irreversible)

alcohol abuse can cause thamine B1 deficiency
cause impaired glucose metabolism and this is bad in the brain

symptoms: opthalmoplegia, ataxia, changes in mental state, coma, death, memory imairment

172
Q

Damage to Broca’s area causes what?

A

Damage to Broca’s area →expressive nonfluent aphasia (trouble expressing language → “individuals know what they want to say, but cannot get it out”)

173
Q

Damage to Wernicke’s area causes what?

A

Wernicke’s aphasia
Wernicke’s area–assigns speech sounds meaning
Damage to Wernicke’s area → receptive, fluent aphasia (trouble interpreting language)
neologisms, real words used meaninglessly; structurally intact speech, typical intonation but lacks content

174
Q

What is the cause of Parkinson’s disease?

A

movement disorder
degeneration of dopaminergic neurons in substantia nigra causing disruption of connection to thalamus motor cortex
symptoms: tremor, rigidity, akinesia, postural instability

usually idiopathic but also associated with mutation of PINK1, parkin and alpha synuclein genes

onset after age 50

175
Q

What accumulations can be found in the dopaminergic neurons before they die in parkinson’s patients?

A

lewy bodies
alpha synuclein accumulation

176
Q

What is the difference between the tremor in parkinsons and cerebellar disease?

A

in parkinsons the tremor is a resting tremor
in cerebellar it is an intention tremor

177
Q

What are the treatments for Parkinson’s

A

SALAD
Selegiline
Anticholinergics
L Dopa
Amantadine–antiviral increases dopamine
Dopamine postsynaptic receptor antagonists

178
Q

What is myasthenia gravis?

A

An autoimmune neuromuscular disease attacking skeletal muscle
type II hypersensitvity, antibodies bind to nicotinic ACh receptors
these Ab also activate complement pathway causing destruction of muscle cells and receptors

symptoms: double vision, ptosis, tiredness throughout day
treatment: acetylcholineesterase inhibitors (neostigmine, pyridostigmine)

179
Q

Carpal tunnel is due to?

A

median nerve compression

180
Q

What is the MOA of riluzole?

A

disease modifying agent
used in motor neuron diseases
for use in mild-moderate disease < 5 year duration
used to treat amyotrophic lateral sclerosis

blocks TTX-sensitive sodium channels, which are associated with damaged neurons
increase astrocyte glutamate uptake
enhance GABA activity

181
Q

What is the cause of Huntington’s disease

A

degeneration of caudate nucleus
AD CAG (glutamine) triplet repeat disease
accumulation of huntingtin protein

chorea, dementia, behavioural disorders

182
Q

What is the cause of Wilson’s disease

A

(rings around eyes)

degeneration of lenticular nucleus
autosomal recessive
abnormal copper accumulation
dystonia, ataxia, subcortical dementia

183
Q

What is a monosynaptic reflex?

A

Reflex arcs that contain only two neurons, a sensory and a motor neuron, are considered monosynaptic. Examples of monosynaptic reflex arcs in humans include the patellar reflex and the Achilles reflex.

184
Q

Which parts of the circle of Willis are the most common sites for atherosclerosis?

A

branch points of the internal carotid and middle cerebral most commonly

Anatomy: several systems (Jenna Goff) (23 decks)

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