Presentation on theme: "Clinical neuroanatomy for CT1s Dr John O’Donovan Friday 8 th June."— Presentation transcript:
Clinical neuroanatomy for CT1s Dr John O’Donovan Friday 8 th June
Basics Neurons of which there are many types, with many functions, make up the nervous system. The nervous system for our purposes comprises the brain, spinal cord and peripheral nerves. Focus for CT1 should be on both clinical and scientific but more so on clinical. The anatomy tends to be bottom up but clinical signs tend to be top down.
The brain in the skull Frontal lobes Temporal lobes Occipital lobes Parietal lobes Limbic lobe/system Cerebellum Pituitary and hypothalamus (hypophysis) Pons, midbrain, medulla oblongata-cranial nerves and nuclei.
Frontal lobe Match them UP? Look at the size of that frontal lobe!
Frontal lobe syndromes Orbitofrontal: disinhibition, witzelsucht, euphoria, lability, poor judgment and poor attention. Frontal convexity: apathetic, indifferent, retarded, perseverating Medical frontal: akinetic, mutism, gait problems and incontinence. Massive frontal lobe syndromes: combination of all four. All a gross oversimplification.
Worth noting the following about cortical lesions Less deficit per volume affected Frequently patients are unaware of extent of deficit, “anosagnosia” Tends to be inconsistent Multimodal deficits eg alexia, need analysis. There is individual variation in cortical function. The neurology is syndrome based and therefore these are by definition imprecise to some extent Clinical presentation also varies by tempo and nature of damage Cortical plasticity means that elementary functions improve better then complex deficits. Cortex is susceptible to global systemic fluctuation, such as delirium Selective cortical lesions tend to cause seizures and multimodal deficits
Other signs Precentral gyrus: face, hand, leg and urinary incontinence if bilateral. Also with unilateral if massive. Mesial aspect: akinesis, perseveration, grasping, “salutatory seizures”, alien hand sign, transcortical motor aphasia, bilateral ideomotor apraxia Lateral aspect: impaired saccades, pure agraphia in dominant hemisphere, contralateral, arm weakness Frontal pole: orbitofrontal as before degree of acquired sociopathy
Frontal lobe summary Motor problems Eye movements on contralateral side Contralateral hemiparesis, face, hand, leg (arm more then leg) Inability to start or stop correctly, akinesis and perseveration Oddities, alien hand, grasping and pure agraphia Non motor problems Motor aphasia: Broca’s Incontinence if bilateral Inability to plan ahead Poor self monitoring and social judgment Acquired sociopathy Dysexecutive Remember caveat about cortical lesions.
Temporal lobes Lateral aspectRemember the hippocampus
Temporal lobe Lanuage Wernicke’s area, receptive aphasia Non language funcions Emotion Memory by means of the hippocampal complex Verbal memory is more left based and visual is more right based. (simplification) Complex partial seizures NB
Temporal lobe 2 Inferomedial Anmesia Bilateral anterior temporal lobe lesions can lead to Kluver-Bucy Syndrome with visual agnosia, hyperoral, tameness, hypersexual, hypomotile and hypermetamorphosis (paying attention to every visual stimulus) Lateroinferior Dominant: transcortical sensory aphasia and word selection anomia, in essence receptive aphasias Non Dominant: Impaired recognition of facial emotional expression.
Temporal lobe 2 Laterosuperior Dominant: pure word deafness and sensory aphasia. Nondominant: sensory amusia and sensory aprosodia. Bilateral lesions of lateral superior aspect Auditory agnosia
Temporal lobe 3 Eye problems Contralateral superior quadrantic anopsia, Meyer’s loop etc. Seizures Temporal lobe both left and right, hippocampus, amygdala and connections are frequent source of complex partial seizures- separate discussion. Non localising signs Auditory hallucinations Complex visual hallucinations
Parietal Lobe Sensory inputMaking sense of it all
Parietal lobe 1 Post central gyrus damage causes contralateral sensory disturbance, pain and paresthesia Mesial aspect in dominant hemisphere can cause transcortical sensory aphasia Lateral aspect Dominant, parietal apraxia, finger agnosia, acalculia, right left disorientation, literal alexia and possibly conduction aphasia. Note Gerstman Syndrome Non Dominant, anosognosia, autopagnosia, spatial disorientation, hemispatial neglect, constructional and dressing apraxia
To simplify Parietal lobes are sensory and put sensory input into context. Dominant lobe injury on lateral aspect can allegedly cause a Gerstman Syndrome. This is a bit of a myth, but a useful one for the MRCPsych.
Gerstman Syndrome Agraphia –can’t read. Acalculia – can’t do arithmetic. Finger agnosia –can’t recognize fingers. Left right disorientation – left verus right Dominant angular and marginal gyrus. Very debatable if it exists, beloved of post graduate examinations.
Occipital lobe Mesial Visual field cut Visual agnosia Visual hallucinations Anton syndrome-cortical blindness without insight into blindness (anosagnosia) Alexia without agraphia- generally also with splenium involvment. Lateral Alexia with agraphia Impaired optokinetic nystagmus Impaired scanning.
John’s simple rules Frontal lobe is ultimately about doing stuff, speaking, walking, planning, studying etc. Temporal lobe all about memory and understanding language. Obviously the receptive language area is beside the ears!, memory is a bilateral function, anything you hear or how you hear it. Parietal lobe is ultimately about sensory input Occipital lobe is about vision Left hemisphere is dominant, any question with language, check dominance.
MCQs Frontal lobes Frontal lobe lesions cause Contralateral sensory problems. Transcortical sensory aphasia Incontinence Witzelsucht Reckless behavior Versive seizures Alien hand phenomena Frontal lobe lesions 2 Being rude to in laws Watching TV all night Perseveration Grasping Primitive reflexes Echopraxia Echolalia Pure agraphia Problems with memory
MCQs Temporal lobes Bilateral temporal lobe lesions cause Disorders of memory Transcortical motor aphasia Amnesia Paraamnestic phenomena Incontinence Contralateral motor weakness May if bilateral cause Kluver-Bucy Syndrome Emotional problems Dominant temporal lobe lesions cause Inferior visual quadrantopia Auditory agnosia Amusia Aprosody Difficulty recognizing when your wife is angry Hallucinations?
MCQs Parietal lobes Parietal lobe lesions cause Motor problems Dressing apraxia Anosagnosia Autopagnosia Alexia Finger agnosia Visual integration problems Dominant parietal lesions always Cause Gerstman Syndrome Contralateral paresthesia Reduced light touch, but preserved propioception on contralteral side. Acalculia Cause hemispatial neglect.
story The four lobes of the brain were friends. Frontal Frank was a leader. He decided what to do and how to do it. He was always talking and always moving around. He made all the decisions and was a dominant personality. Tempermental Tim on the other hand, was always listening out for what anybody said about him and he had a prodigious memory but was prone to being moody and sometimes would seize up with odd feelings, which he could not explain very well. Frank used to go out with Pretty Parie but he broke up after being unable to satisfy her sensory needs. On top of which, despite dominating Frank, she did not read, add up, know her left from right or ever recognize her fingers and he found it hard to deal with her constant whining about her right side not being properly dressed and neglecting him all the time. Ultimately he went to tempermental Tim for advice who told him to speak with Occy who had a reputation as a bit of a visionary. Occy told Frank that he couldn’t see what was in it for him and to have a bit of a look around on the other side. Frank never took advice well and ended up beating Occy half blind, but suffered a stroke affecting his arm in particular and ended up mute and incontinent. This upset Tim so badly that he went into status epilpticus and lost his memory for everything. Pretty Parie meanwhile continued trying to make sense of it all.
Occipital lobe lesions If dominant Cause ipsilateral hemianopsia Can cause colour desaturation. Can cause alexia Mean that you can no longer drive May cause visual hallucinations If bilateral Can cause cortical blindness Are normally caused by pump failure. Can occur in prion disease Impair the pupil response Can cause Balint Syndrome
And now for something different Neuroanatomy of vision Neuroanatomy of the spinal cord Neuroanatomy of the basal ganglia and cerebellum Neuroanatomy of the peripheral nerves
Pupils 4 parts Optic nerve-pretectal area in midbrain Pretectum to Edwinger Westphal nucleus (parasympathetic nucleus of !!! Occulomotor nerve) Edwinger Westphal nucleus bilateral to ciliary ganglion Ciliary ganglion to constrictor muscles of iris
Light near dissociation Argyll Robertson Pupil, syphilitic eye disease, very rare, lesion site around the aqueduct. “the prostitute accomodates but does not react” Holmes-Adie tonic pupil With arreflexia Adie Syndrome, prevalence is 1:500, degeneration of ciliary ganglion, other name is tonic pupil. Parinaud Syndrome, rostral midbrain stroke, presumably from damage to midbrain Remember 80% of the ciliary ganglion response is for accomodation, not light.
Dilated pupil from occulomotor palsy - occulomotor nerve, ptosis, down and out with mydriasis. Remember parasympathetic fibres run on the outside of the nerve and are susceptible to trauma. Coning of the brain, trauma, ptuitary lesions, PICA aneurysms. Axonal palsies from diabetes and vasculitis tends to be pupil sparing.
Drugs that cause mydriasis Atropine Hyoscine Scopolamine Tropicamide All anti cholinergics Anti cholinergics-not drugs with weak anti cholinergic effects.
Congenital Anywhere in sympathetic chain Hypothalamus C8/T1 root Pancoast tumours, apex of lung
Visual pathways 2 Tends not to be asked. Generally very basic, remember to draw the pathway. Pituitary lesions cause bitemporal hemianopsia Occipital cause a contralateral field cut, left occipital lesions cause right sided hemianopsia.
MS eye signs, optic neuritis and internculear opthalmoplegia (dissociated nystagmus)
Eye MCQs a normal pupil response Daylight causes mydriasis Both pupils are equal in size Both respond consensually Two cranial nerves are used Second relay centre is in the pons The ciliary ganglion is sympathetic Accomodation is to light as 2:1 Argyll Robertson pupils Are always pathological Can be associated with an absent ciliospinal reflex Don’t react to light React quickly to accomodation Are common with HIV infection Are similar to Holmes-Adie pupils
Eye MCQs Match the following Growing hands, feet and diabetes Young woman with weak left leg and double vision Smoker with a painful armpit Cortical blindness Xanthochromia Possible answers Compressive third nerve palsy. Bitemporal hemianopsia Horner’s Syndrome Old variant CJD Multiple sclerosis Myasthenia gravis Relative afferent pupil defect.
Spinal cord and brainstem
Use cranial nerve nuclei to find lesion level. Remember deccusation in the pyramids of the medulla oblongata-crossed syndromes. Lateral medullary syndrome frequently sneaks in and therefore must be known. Remember pons-trigeminal nerve, pontine pupils, CPM-central pontine myelinosis Unlikely to be asked specifics
Syringomyelia/Bulbia Hole in central spinal cord filled by CSF Results in weakness-combined lower and upper motor neuron signs Dissociated sensory loss-meaning that it affects spinothalamic tracts with anaesthesia and absence of temperature perception. Can result in Charcot Joints, most commonly in hands and shoulders Classically shows a cape distribution sensory loss Syringobulbia is when it extends into the bulbar area and causes cranial nerve and brainstem signs. Norallly lower cranial nerves and sometimes trigeminal.
Brown-Sequard Syndrome Hemitransection of cord Same side as lesion UMN weakness and posterior column problems Contralateral side loss of pain and temperature (spinothalamic)
Cord transection Rarely asked as question In general, below lesion spasticity and weakness Plantar externsor and clonus Neurogenic bladder and bowel Lesion level guides disability Cord level does not equate precisely to root level
Peripheral nerves Highly unlikely to be asked as a question. Some basics- peripheral nerve lesions or lower motor neruon lesions cause arreflexia at level of lesion, atrophy, weakness and fasiculations. Can be subdivided into many types of lesion but simply put, either axonal or demyelinating such as AIDP. Axonal lesions tend to occur in vascular process and cause more gross atrophy.
Peripheral neuropathy Glove and stocking Longest nerves first (sciatic!), begins in feet. Common causes of painful peripheral neuropathy diabetes and drink, B12. Commonest cause of peripheral neuropathy worldwide is leprosy. Acute flacid weakness-AIDP, GBS
MCQs on cranial nerves, spinal cord and peripheral nerves Bells palsy is a lesion of the trigeminal nerve. The afferent arc of the corneal reflex is in the maxillay branch of the trigeminal nerve Swallowing requires an intact hypoglossal nerve Bilateral LMN facial palsies can occur in sarcoid Brown Sequard syndrome results in ipsilateral spinothalamic function loss UMN lesions cause fasiculations A syrinx of the thoracic cord can cause bladder problems Following cause peripheral neuropathy Lead Diabetes Acute intermittent porphyria Metronidazole Alcohol B12 deficiency Cryoglobulinaemia Lithium
Cerebellum and basal ganglia
Basal ganglia and cerebellum Functions are ultimately to provide smooth and effective movements. Much greater role then simply movement, needed for cognition, emotion, reward networks, executive functioning. Multiple feedback loops between cortex and basal ganglia, allows cortex and basal ganglia to self monitor, to some extent.
Cerebellar Signs Ipsilateral Ataxia Rebound Slow reflexes Nystagmus Tremor Difficulty with rapidly pronating/supinating movements- dysdiadokinesi Dysarthria Hypotonia Midline-vermian commonly from alcohol Central ataxia Dysarthria
Causes of cerebellar disease Alcohol Drugs-intoxication eg phenytoin toxicity Toxins Hypoxia Stroke Trauma Celiac disease Paraneoplastic with breast/ovarian in particular Congenital-SCAs, pure cerebellar degenerations Congenital
The basal ganglia PathwaysAnatomy
Functions Motor Cognitive Emotional Damage in any area of basal ganglia can produce problems in those three domains.
Cognitive Sub cortical dementias Slowness Bradyphrenia Psychomotor retardation Apathy Reduced language generation Secondary frontal effects
Emotional Obsessional (sometimes) Affective instability/frontal Depression-very common and can be severe Abulia, akinesis and apathy
Motor Abnormality of speed of movement, generally bradykinesia as in Parkinson’s but can be accelerated as in HD or hemibalismus Tremor Chorea Dystonia Athetotis Dystonia Hemibalismus Also dysarhtria and clumsiness
Parkinson’s Disease tremor rest 4-6hz Bradykinesia Poor postural reflexes Festinant gait Response to dopa Presents as assymetric
Wilson’s Disease Very rare Metabolic AR genetics Check condanguinity Liver disorder Copper metabolism goes wrong Clinically, liver disease, eye disease and dystonic, parkinsonian illness with marked axial and bulbar roblmes Neuropsychiatric problems,global cognitive decline and personality alterations
MCQs In cerebellar disease Signs are contralateral Reflexes are pendular Hypertonia is the norm DRPLA is a common cause There may be malabsorbtion There are cognitive and affective changes Alcohol should be avoided Rebound is seen Prosody is affected In movement disorders Cognition is always affected. Depression is common OCD may be associated with tics Parkinson’s is normally assymetric in onset Parkinson’s always responds to dopa Parkinson plus syndromes have a good prognosis Chorea in a forty year old alcoholic with poor impulse control is worrying HD shows anticipation HD is a trinucleotide repeat