Brian Flashcards
impulsiveness and loss of inhibition
what lobe
Frontal lobes lesions expressive (Broca's) aphasia: located on the posterior aspect of the frontal lobe, in the inferior frontal gyrus. Speech is non-fluent, laboured, and halting disinhibition perseveration anosmia inability to generate a list
temporal lobe injury
Temporal lobe lesion
Wernicke’s aphasia: this area ‘forms’ the speech before ‘sending it’ to Brocas area. Lesions result in word substituion, neologisms but speech remains fluent
superior homonymous quadrantanopia
auditory agnosia
prosopagnosia (difficulty recognising faces)
Hallucinations can occur in temporal lobe seizures
metallic smell an taste
occipital lobe lesions
Occipital lobe lesions
homonymous hemianopia (with macula sparing)
cortical blindness
visual agnosia
pariteal lobe lesions
Parietal lobe lesions sensory inattention apraxias astereognosis (tactile agnosia) inferior homonymous quadrantanopia Gerstmann's syndrome (lesion of dominant parietal): alexia, acalculia, finger agnosia and right-left disorientation
cerebellum lesions
Cerebellum lesions
midline lesions: gait and truncal ataxia
hemisphere lesions: intention tremor, past pointing, dysdiadokinesis, nystagmus
subdural bleed looks like what
crescent shap e
subdural bleed caused by what
rupture of bridging veins
stylohyoid innervated by what nerve
facial nerve
The hypoglossal nerve emerges anterior to the olive of the medulla oblongata. CNIX-XI emerge posterior to the olive
true
Anterior to the olive of the medulla is the correct answer for the hypoglossal cranial nerve. In this case, the isolated hypoglossal nerve lesion is most likely due to the base of skull meningioma found on brain imaging. The tongue always deviates towards the side of the hypoglossal nerve lesion.
Anterior midbrain is incorrect as this is the exit for cranial nerve 3.
Pons is incorrect as this is the exit of cranial nerve 5 from the brainstem.
Pontine-medullary junction is incorrect as this is the exit of cranial nerves 6 to 8.
Posterior midbrain is incorrect as this is the exit of cranial nerve 4, which has the longest cranial course of all the cranial nerves.
oxytocin is made where in the hypothalamus
Oxytocin is produced by the paraventricular nucleus of the hypothalamus
Mammillary bodies of the hypothalamus are important for recollective memory. Damage to these bodies, for example in thiamine deficiency in Wernicke-Korsakoff syndrome, leads to impairment in memory.
ok sign
anterior interosseous nerve
cranial nerve 7 palsy also called bells palsy is associated with what
glandular fever - EBV
nerve with longest length
he trochlear nerve has the longest intracranial length of any of the cranial nerves
The patient develops binocular vertical and torsional diplopia.
When testing the patient’s cranial nerves he has vertical diplopia, worsened by looking downwards and inwards.
The genitofemoral nerve divides into two branches as it approaches the inguinal ligament
he genital branch passes anterior to what artery at the deep inguinal canal
The genital branch passes anterior to the external iliac artery through the deep inguinal ring into the inguinal canal. It communicates with the ilioinguinal nerve in the inguinal canal (though this is seldom of clinical significance).
rise in ICP causes fall in what
The cerebral perfusion pressure (CPP) is defined as being the net pressure gradient causing blood flow to the brain. The CPP is tightly autoregulated to maximise cerebral perfusion. A sharp rise in CPP may result in a rising ICP, a fall in CPP may result in cerebral ischaemia. It may be calculated by the following equation:
CPP= Mean arterial pressure - Intra cranial pressure
Following trauma, the CPP has to be carefully controlled and the may require invasive monitoring of the ICP and MAP.
Temporal lobe (HEAD) seizure
Hallucinations (auditory/gustatory/olfactory), Epigastric rising/Emotional, Automatisms (lip smacking/grabbing/plucking), Deja vu/Dysphasia post-ictal)
Lip smacking + post-ictal dysphasia are localising features of a temporal lobe seizure
frontal lobe ( motor) seizure
vHead/leg movements, posturing, post-ictal weakness, Jacksonian march( clonic movements travelling proximally) indicates frontal lobe epilepsy)
A 70-year-old man presents to the emergency department. He states that on his left hand he had twitching on the left side of his mouth which spread to his whole face. The patient was aware throughout and was not confused afterward. His neurological examination was normal.
Parietal lobe (sensory) - seizure
parenthesis
Occipital lobe (visual) seizure
floaters and flashes
Where is the vomiting centre located?
medulla
ABC’s of Non- GI causes of vomiting
Acute renal failure Brain (Increased ICP) Cardiac (Inferior MI) DKA Ears (labyrinthitis) Foreign substances (Tylenol, theo, etc) Glaucoma Hyperemesis Gravidarum Infections (pyelonephritis, meningitis)
receptors for vomiting located where
Labyrinthine receptors of ear (motion sickness)
Over distention receptors of duodenum and stomach
Trigger zone of CNS - many drugs (e.g., opiates) act here
Touch receptors in throat
posterior communicating artery aneurysm causes what nerve palsy
3rd
astrocytes are responsible for what
removal of excess potassium ions
Important for meLess important
The greater petrosal nerve may be injured and carries fibres for
lacrimation
Neuropraxia
Nerve intact but electrical conduction is affected
Full recovery
Autonomic function preserved
Wallerian degeneration does not occur
Axonotmesis
Axon is damaged and the myelin sheath is preserved. The connective tissue framework is not affected.
Wallerian degeneration occurs.
Neurotmesis
Disruption of the axon, myelin sheath and surrounding connective tissue.
Wallerian degeneration occurs.
Wallerian Degeneration
Axonal degeneration distal to the site of injury.
Typically begins 24-36 hours following injury.
Axons are excitable prior to degeneration occurring.
Myelin sheath degenerates and is phagocytosed by tissue macrophages.
Nerve repair
Neuronal repair may only occur physiologically where nerves are in direct contact. Where a large defect is present, the process of nerve regeneration is hampered. It may not occur at all or result in the formation of a neuroma. Where nerve regrowth occurs it is typically at a rate of 1mm per day.
full recovery of function 12 months
where does the spinal cord terminate in adults
L1
features of sciatic nerve lesion
Features of sciatic nerve lesion
motor: paralysis of knee flexion and all movements below knee
sensory: loss below knee
reflexes: ankle + plantar lost, knee jerk intact
thalamus
ucleus/nuclei Function
Lateral geniculate nucleus Visual signals
Medial geniculate nucleus Auditory signals
Medial portion of the ventral posterior nucleus (VML) Facial sensation
Ventral anterior/lateral nuclei Motor
Lateral portion of the ventral posterior nucleus Body sensation (touch, pain, proprioception, pressure, vibration)
Dopamine agonists (often used in Parkinson’s disease) have a risk of impulse control or obsessive disorders (such as excessive gambling or hypersexuality)
pramipexole
