Neuro LEAP Past Paper PDF

OS 202: HUMAN BODY AND MIND 1: INTEGRATION AND CONTROL SYSTEMS NEURO LEAP UPCM 2029 | Dr. | LU A.Y. 20-20 OUTLINE CORTICOSPINAL TRACT I.​ Station 1:...

OS 202: HUMAN BODY AND MIND 1: INTEGRATION AND CONTROL SYSTEMS NEURO LEAP UPCM 2029 | Dr. | LU A.Y. 20-20 OUTLINE CORTICOSPINAL TRACT I.​ Station 1: VI.​ Station 6: BE FAST Anti-Herniation VII.​ Station 7: II.​ Station 2: Black Box Demyintindihan: OGK III.​ Station 3: In Pain in the VIII.​ Station 8: Decuss8 Membrane IX.​ Station 9: Time is Brain IV.​ Station 4: Mal4mation X.​ Station 10: Dis/Cord V.​ Station 5: Space Occupying Lesson A.​ Subtopic B LEARNING OBJECTIVES 1.​ Explain the rostrocaudal progression of brain herniation 2.​Explain how the different areas of the cerebral cortex are affected in aphasia, anomia, seizures, and dementia 3.​Recognize constellations of signs and symptoms of cranial neuropathies 4.​Explain how ruptured aneurysms cause headache 5.​Explain the role of the dura mater and middle meningeal arteries in migraine 6.​Explain how visual field defects occur with lesions of the visual system 7.​Trace the corticospinal and corticobulbar tracts and correlate with different patterns of weakness I.​ STATION 1: ANTI-HERNIATION A.​ CASE ​ General Information: ○​ M.V., a 20/M, R-handed, from Marinduque ​ Chief Complaint: ○​ Decrease in sensorium ​ Capsule History: ○​ Known case of TB last October, but only compliant with TB medications for 2 months ○​ Four days prior to consult, patient had a seizure episode with associated occasional headaches ○​ Four hours prior to admission, complaints of headache and sudden decrease in sensorium ​ Pertinent PE: ○​ No eye opening to pain, no verbal output, decorticates ○​ Pupils 5mm/4mm nonreactive to light, no Dolls, sluggish corneals, weak gag DORSAL COLUMN MEDIAL LEMNISCUS PATHWAY B.​ TASK ​ Specimen: cut slices of the brainstem ​ Arrange the brainstem slices from most rostral to caudal and take a photo. ​ Trace the corticospinal tract and medial lemniscus pathways in the brainstem slices Trans # TG#: Surname 1, Surname 2, etc. TH: Surname 1 of 8  C.​ CLINICAL INTERPRETATION ​ Potential Diagnosis ○​ Tuberculosis Meningitis (TBM) ​ History of TB: The patient’s history of poor TB medication adherence could cause the bacterium to spread to the central nervous system, leading to meningitis ​ Gradual Onset of Symptoms: Headaches, seizures, and altered consciousness show signs of CNS involvement ​ Brainstem Involvement: Chronic inflammation forms granulomas in the meninges or can obstruct CSF flow (hydrocephalus), leading to increased intracranial pressure, causing direct irritation and compression to the brainstem (as shown by symptoms like decorticate posturing, no dolls, sluggish corneals, and weak gag reflex) ​ Differential Diagnoses ○​ Cerebral Tuberculoma: though also caused by TB, tuberculomas C.​ CLINICAL INTERPRETATION are more localized in the brain parenchyma and show acute onset ​ Potential Diagnosis of symptoms ○​ Brainstem stroke ○​ Sepsis with Ecelopathy: can lead to decreased sensorium, but is ​ Decreased sensorium: A stroke involving the brainstem can usually associated with systemic signs of infection like fever and impair consciousness and lead to altered sensorium. tachycardia (not reported in the case) ​ Cranial nerve involvement: The ptosis (drooping of both eyes) ○​ Metabolic or Electrolyte Imbalance: though unlikely, but and facial palsy (right-sided) suggest involvement of cranial metabolic and electrolyte disturbances can be the reason for nerves, which are housed in the brainstem. decreased consciousness and seizures ​ Asymmetric motor response: Spontaneous movement of the II.​ STATION 2: BLACK BOX right extremities more than the left points to a lesion affecting motor pathways in the brainstem, possibly affecting the A.​ CASE corticospinal tract. ​ General Information: ​ Common arteries involved in a brainstem: ○​ O.E., 62/F, R-handed, from Pasay ​Midbrain ​ Chief complaint ○​ Posterior Cerebral Artery ○​ Decrease in sensorium ​Pons ​ Capsule History: ○​ Basilar Artery branches ○​ 4 hours prior to consult, patient was seen on the floor with no eye ​Medulla opening ○​ Vertebral Artery & Posterior Inferior Cerebellar Artery ○​ Only moans when called, with minimal movement of the ​ Differential Diagnosis extremities ○​ Hemorrhagic Stroke: If there is bleeding in the brain, it can cause ○​ This prompted consult in PGH similar symptoms as an ischemic stroke but with potential ​ Pertinent PE: additional signs, such as increased intracranial pressure, which ○​ Eye opening to name calling, moans to pain, inconsistently can contribute to changes in sensorium. The sluggish reflexes follows and asymmetric movement could also be due to mass effect from ○​ Pupils 2mm isocoric sluggishly reactive to light an expanding hematoma. ○​ Ptotic both eyes, no horizontal movement on both eyes, sluggish ○​ Severe hypoglycemia or metabolic disturbances: Although less corneals on the right likely given the focal neurologic findings, it could also cause ○​ Right peripheral facial palsy altered sensorium. However, the focal neurologic signs (facial ○​ Spontaneous movement of the right extremities more than the palsy, ptosis, asymmetric motor movement) are more specific to a left CNS lesion. ○​ Brain tumor or space-occupying lesion: This is also a potential consideration, especially if the patient’s symptoms have been evolving over time (though the acute onset would make this less likely). III.​ STATION 3: IN PAIN IN THE MEMBRANE D.​ CASE ​ Specimen: uncut brain still encased in dura mater, dura mater (cut), and human heads with calvaria removed ​ General Information: ○​ J.D., 22, R-handed, from Manila; ​ Chief Complaint: Trauma ​ Capsule History: B.​ TASK ○​ 2 hours prior to admission, drunk patient had a vehicular crash ​ Specimen: cut slices of the brainstem with no helmet, loss of consciousness and epistaxis, no noted BRAINSTEM vomiting, seizures. Patient was then brought to our institution. ​ Pertinent PE: ​ Arrange the brainstem slices for most rostral to caudal and take a ○​ No eye opening to pain, no verbal output, localizes to pain photo ○​ Pupils 2 mm isocoric, briskly reactive to light ○​ Intact dolls, intact corneals, intact gag ○​ Withdraws to pain more on the right ○​ (+) sustained clonus on the left RULE OF 4’S: 4 STRUCTURES IN THE MIDLINE BEGIN WITH THE LETTER M CLINICAL INTERPRETATION ​ Choose any one of the brainstem rule of 4’s and digitally markup ​ Based on the scans, there is an epidural hematoma or hemorrhage. your brainstem slice photos This epidural is due to the lemon shape of the bleed, which is usually limited by the sutures in the skull. ​ This may have occurred because of the vehicular crash with no helmet, causing head trauma to the patient. E.​ TASKS OS 202 Topic Name 2 of 8  IDENTIFICATION OF STRUCTURES ​ Middle Meningeal Artery ​ Dura Mater Over Superior Sagittal Sinus ​ Superficial Temporal Artery IN PAIN IN THE MEMBRANE ​ The epidural hematoma, being adjacent to the protective membranes, contributes to “pain in the membrane.” A.​ CLINICAL INTERPRETATIONS ​ The middle meningeal artery burrows into pain-sensitive structures ​ Potential Diagnosis and its dilation causes substance P and neurokinin A release, both ○​ Acute Intracerebral Hemorrhage (ICH) of which are involved in pain modulation. ​ Hyperdense Lesion in the Left Frontal Lobe: likely due to a IV.​ STATION 4: MAL4MATION rupture of the middle cerebral artery (MCA) ​ Specimens: axially cut brains ​ L>R Hemiparesis & Speech Impairment (Aphasia): likely due to the localization of the lesion to the left hemisphere (dominant D.​ CASE side), consistent with the hemorrhage seen in the CT scan ​ General Information: ​ Sustained Clonus & Hyperreflexia on the R side: indicative of ○​ N.S., 29/F, R-handed, from Rizal an upper motor neuron lesion ​ Chief complaint: no verbal output ​ Sudden Onset with Vomiting and Collapse: indicative of an ​ Capsule History: acute event, likely a hemorrhagic stroke ○​ 11 hours prior to consult, patient was seen on the floor with pool ​ Differential Diagnoses of vomitus, right-sided weakness, and no verbal output. ○​ Hypertensive Intracerebral Hemorrhage (ICH): less likely given ○​ Patient was then brought to our institution. the px’s young age, but possible ​ Pertinent PE: ○​ Arteriovenous Malformation (AVM) Rupture or Aneurysm: highly ○​ BP on arrival 120/80 suggested by the CT angiography findings regarding the ○​ Awake, no verbal output, follows abnormal vasculature ○​ Pupils 2 mm isocoric reactive to light, right shallow nasolabial fold ○​ Cerebral Venous Sinus Thrombosis (CVST): less likely due to the MMT 5/5 L, 4/5 R, DTRs +2 L, +3 R, (+) sustained clonus on the R acute focal neurological signs and imaging findings, which could cause similar symptoms, including vomiting and focal deficits, through increased intracranial pressure. V.​ STATION 5: SPACE OCCUPYING LESSON ​ Specimens: sagittal slices of the cerebrum B.​ CASE ​ General Information: ○​ L.A., 59/F, R-handed, from Bulacan ​ Chief complaint: ○​ Headache ​ Capsule history: ○​ 1 month history of left-sided headache with occasional seizure episodes described as blank stares, upward rolling of the eyeball, E.​ TASKS and generalized tonic-clonic seizure of the right extremities ​ Pertinent PE: BRAIN SLICES ○​ Awake, oriented, follows ​ Peruse both the imaging of the jumpoff case as well as the axial ○​ No craniopathies brain slices; take photos of the brain slices that correspond to the ○​ MMT 5/5 on the L, 4/5 on the R lesions that would cause the patient's neurological deficits ODD NUMBER TEAMS ​ ODD number teams: draw/color red where the lesion(s) is/are on the photos to approximate what you saw on the scans closely EVEN NUMBER TEAMS ​ EVEN number teams: arrange yourselves to replicate the visual system from optic nerves to optic tracts for both eyes and all 4 quadrants, and ask someone to take your photo OS 202 Topic Name 3 of 8  C.​ TASKS A.​ CASE ​ General information BRAIN SLICES ○​ M.L., a 74/F, R-handed, from Las Pinas ​ Peruse both the imaging of the jumpoff case as well as the axial ​ Chief complaint brain slices; take photos of the brain slices that correspond to the ○​ Facial asymmetry lesions that would cause the patient's neurological deficits ​ Capsule history ○​ Day of consult, noted sudden onset of left-sided facial drooping, EVEN NUMBER TEAMS and L-sided weakness. Patient was then brought to our ER for co ​ EVEN number teams: draw/color red where the lesion(s) is/are on management. the photos to approximate what you saw on the scans closely ​ Pertinent PE ○​ (+) irregularly irregular rhythm ○​ Awake, oriented, follows commands ○​ Left homonymous hemianopia, pupils 2 mm brisk, right preferential gaze ○​ (+) dysarthria, left central facial palsy, left hemiplegia B.​ TASKS BRAIN SLICES ​ Peruse both the imaging of the jumpoff case as well as the coronal brain slices; take photos of the brain slices that correspond to the lesions that would cause the patient's neurological deficits ODD NUMBER TEAMS ​ ODD number teams: arrange yourselves to replicate the visual system from optic nerves to optic tracts for both eyes and all 4 quadrants, and ask someone to take your photo ​ Pertinent PE ○​ (+) irregularly irregular rhythm ​ Indicates atrial fibrillation, which could have led to clot formations that obstructed vessels in the brain (e.g. middle cerebral artery) ​Possible cardioembolic stroke, which is also characterized by sudden weakness and facial droop ○​ Awake, oriented, follows commands ​ No problems with higher cortical function (no damage to prefrontal cortex) ○​ Left homonymous hemianopia ​ Lesion at the right optic nerve before the Chiasma ○​ pupils 2 mm brisk, ​ No problem with pupillary reflex ○​ right preferential gaze ​ Problem with CN VI (Lateral rectus) and CN III (medial rectus) ○​ (+) dysarthria, left central facial palsy, left hemiplegia ​ Right somatosensory cortex is damaged affecting face and body ​ Shade all the arterial territories that you can depict to teach yourselves and others the blood supply of the brain (including close D.​ CLINICAL INTERPRETATIONS up pictures of the midbrain and medulla) ​ Potential Diagnosis ○​ Space-occupying lesion (SOL) in the left hemisphere: ​ Headache: Likely due to increased intracranial pressure or irritation of surrounding tissues (e.g., meninges) ​ Seizures: Focal seizures with blank stares and upward eye movements suggest involvement of the left hemisphere (likely temporal or frontal lobe) ​ Secondary generalization: Tonic-clonic seizures of the right extremities indicate the spread of seizure activity to both cerebral hemispheres ​ Right-sided weakness (MMT 4/5): Indicates a contralateral motor deficit, pointing to a lesion in the left hemisphere affecting motor control pathways ​ Differential Diagnoses ○​ Brain tumor (primary or metastatic): ​ Tumors such as gliomas, meningiomas, or metastases can present with similar symptoms due to mass effect ​ Absence of acute onset favors a slow-growing tumor rather VII.​ STATION 7: DEMYINTINDIHAN: OGK than an acute process. ​ Specimens: dissected cerebral white matter, hemisphere with ​ Tumors may cause headaches, focal neurological deficits corpus callosum (weakness, aphasia, etc.), and seizures (due to irritation of ​ General information: RH, 46/F, R-handed, from Laguna cortical areas or mass effect on adjacent structures). ​ Chief complaint: Right LE weakness ○​ Cerebral abscess: ​ Capsule history: ​ Infection leading to an abscess can cause similar symptoms; ​ Pertinent PE: MRI with contrast would differentiate between a tumor and abscess based on enhancement patterns C.​ DEMYELINATING LESIONS ○​ Chronic subdural hematoma: ​ Info ​ Typically presents with headache and focal deficits, but less likely in this case due to the seizure activity and absence of DAWSON’S FINGERS trauma history ○​ Stroke (ischemic or hemorrhagic): ​ Strokes can present with headache, weakness, and seizures, but these symptoms are more acute in onset, unlike the patient's gradual progression VI.​ STATION 6: BE FAST ​ Specimen: coronal sliced cerebrum OS 202 Topic Name 4 of 8  ○​ The onset of TM is sudden, taking hours to days, with rapid D.​ VITAMIN D IN NEUROLOGY progression of symptoms over days to weeks. On the other hand, ​ Current research shows that vitamin D is necessary in maintaining MS has a more gradual or stepwise progression of symptoms neuronal health and in the regulation of brain development and over the years such as the patient’s case. function ​ Vitamin D is reported to have an important role in the regulation of ​ Acute Disseminated Encephalomyelitis (ADEM) neurotrophic factors such as neuron growth factor (NGF) ○​ Also referred to as post-infectious encephalomyelitis ​ The antioxidant properties of vitamin D also plays a role in the ​ Most cases follow a viral or bacterial infection, although the detoxification in the cells of the nervous system causative agent is not always identified ​ Vitamin D also plays a role in maintaining calcium homeostasis in ○​ An acute, rapidly progressive autoimmune process neurons, mitigating the risk of excitotoxicity (i.e. nerve damage due ○​ Epidemiology: Predominantly occurring in children and young to excessive stimulation) adults with mean age of onset of 3.6-7 years, with no differences ​ Low concentrations of 25-hydroxyvitamin D is linked with the onset in sex and progression of neurodegenerative diseases such as Alzheimer’s ○​ Characterized by demyelination in the brain and spinal cord as disease a result of inflammation that occurs in response to a preceding E.​ CASE infection or immunization ○​ May also occasionally affect the optic nerve ​ General Information: ○​ Presents a specific histopathology that differentiates it from MS ○​ R.H., 46/F, R-handed, from Laguna ​ Perivenous demyelination with an accumulation of florid ​ Chief complaint: inflammatory cells, including lymphocytes, macrophages, and ○​ Right Lower Extremity Weakness microglial cells ​ Capsule history: ○​ Pathology is typically bilateral and polyfocal with deep gray ○​ 6 years prior to consult, noted with blurring of vision on the right matter involvement eye with rapid progression to loss of vision with no improvement. ○​ Onset is acute and rapidly progressive within days characterized 3 years prior to consult, noted with new onset ascending by seizures, diminished sensation, tingling, and weakness of numbness and weakness on the bilateral lower extremity extremities weakness with spontaneous resolution. 1 week prior to consult, ○​ Other signs and symptoms include: with new onset progressive numbness and right lower extremity ​ Altered mental status weakness hence admission. ​ Paraparesis ​ Pertinent PE: ​ Tetraparesis ○​ Awake, oriented, follows ​ Oculomotor dysfunction ○​ Pupils 3mm isocoric briskly reactive to light, no craniopathies ○​ Most cases are monophasic (only one single event) ○​ Hypotonic bilateral lower extremity ○​ Clinical severity may fluctuate within 3 months ○​ MMT 0/5 right lower extremity, others unremarkable ○​ Less likely to be the direct cause of the case due to the ○​ Last normal sensory on T6 progressive onset of signs and symptoms taking multiple years, as opposed to the acute onset of ADEM. Additionally, ADEM usually occurs only once, whereas the patient’s case is recurring. VIII.​ STATION 8: DECUSS8 ​ Specimens: half brains (hemispheres) F.​ CASE ​ General Information: ○​ F.J., 44/M, R-handed, from Nueva Ecija ​ Chief complaint: ○​ Headache ​ Capsule history: ○​ 1 year of holocranial headache associated with blurring of vision on temporal fields of both eyes without any other symptoms. Worsening of symptoms prompted consult at our institution. CLINICAL INTERPRETATION ​ Pertinent PE: ​ Potential Diagnosis ○​ Awake, oriented, follows ○​ Multiple Sclerosis (MS) ○​ Bitemporal hemianopia, no other craniopathies ​ An auto-immune inflammatory that damages myelinated axons ○​ No sensorimotor deficits in the central nervous system. ​ Right Lower Extremity Weakness: ​ Blurring of Vision and Vision Loss: Visual impairment is a key manifestation of MS that occurs in the setting of optic neuritis. Optic neuritis in MS usually involves unilateral vision loss, with pain on eye movement. Myelin sheath covering the optic nerve may be affected in MS, which leads to optic neuritis and vision loss. ​ Initial bilateral lower extremity weakness and resolution can be explained by remyelination post-damage but incomplete repair of myelin sheath ​ Subsequent attacks will lead to plaque formation resembling scarring, leading to axonal death, thus termination of signals in the affected region. ​ Axonal death can result in weakness, presenting as hemiparesis and numbness as synaptic connections are disrupted. G.​ TASKS DIFFERENTIAL DIAGNOSIS COMMISSURAL FIBERS ​ Transverse Myelitis (TM) ○​ Transverse myelitis is a neurological disorder caused by inflammation of the spinal cord. When the spinal cord gets inflamed, this inflammation can damage the insulating material, called myelin, that covers nerve cell fibers. ○​ Similarities with the patient’s case: ​ TM is characterized by ascending numbness and bilateral lower extremity weakness, such as the patient’s case 3 years ago. ​ TM often presents with motor deficits, progressive R LE weakness, and a defined sensory level, such as the patient’s case (T6) ○​ Relapsing course of the case indicates disease is chronic and demyelinating (such as MS), whereas TM is typically monophasic and only has one episode. ○​ Optic neuritis (6 years ago) indicates a systemic demyelinating disorder, unlike TM which does not usually cause optic nerve involvement ○​ TM symptoms often do not resolve completely. Spontaneous resolution of B LE involvement is more consistent with MS ​ Corpus callosum relapsing-remitting ○​ Most prominent, biggest example of commissural fiber OS 202 Topic Name 5 of 8  ○​ Connects right and left hemispheres of temporal, frontal, parietal, understand other people's beliefs or empathize with people and occipital lobes ​ Parahippocampal Gyrus ○​ Parts: genu (most anterior), splenium (most posterior), body ○​ Most medial portion of the temporal lobe, anterior and inferior (connects genu and splenium) continuation of the cingulate gyrus ​ Anterior commissure ○​ Thin and small structure that may be missed depending on how the brain is cut. ○​ Landmark for basal nucleus of Meynert which is an important structure for learning ○​ Anterior fibers connect olfactory bulb and nuclei ○​ Posterior fibers connect middle and inferior temporal gyri ​ Posterior commissure ○​ Technically not part of cerebral hemisphere ○​ Found in diencephalon (brainstem) ○​ Interconnects pretectal nuclei which has a role for mediating consensual pupillary reflex ○​ Marks the caudal extent of the third ventricle ○​ Marks the rostral extent of the cerebral aqueduct PROJECTION FIBERS ​ Connect the cerebral cortex with more caudal structures in the central nervous system, like the thalamus, brainstem, and spinal RATIONALE OF DECUSSATION cord ​ ​ Axons that send either ascending or descending signals and travel IX.​ STATION 9: TIME IS BRAIN within the limbs of the internal capsule ​ Specimen: model brain that can be taken apart into 9 pieces X.​ STATION 10: DIS/CORD ​ Specimen: uncut brain with spinal cord up to cauda equina A.​ CASE ​ General Information: ○​ S.A., 48/F, from Bulacan, known case of Neurofibromatosis type 2 ​ Chief Complaint: ○​ Difficulty ambulation ​ Capsule History: ○​ 2 months prior to consult, noted with decreased sensation on bilateral lower extremities with associated lower extremity weakness the day prior to consult ​ Pertinent PE: ○​ Awake, oriented, follows ○​ No craniopathies ○​ MMT right lower extremity 0/5, rest normal 5/5 ○​ Sensory deficit to pain/temperature on the right lower extremity ○​ Sensory deficit to proprioception on the left lower extremity ​ Corona radiata (Descending and Ascending fibers) ○​ Fan shaped sheet ○​ Superiorly its fibers diverge anteroposteriorly and transversely to reach the cerebral cortex ○​ inferiorly its fibers converge to form internal capsule ​ Internal capsule (Parts) ○​ L-shaped in coronal view ○​ Superiorly continuous with corona radiata ○​ Inferiorly continuous with crus cerebri Table 1. PROJECTION FIBERS DESCENDING ASCENDING FIBERS PART FIBERS (from thalamus) Anterior thalamic B.​ TASK Frontopontine Short Anterior limb radiation ​ Neurological Deficits: Corticonuclear - Genu ○​ Motor strength of 0/5 on right lower extremity (flaccid paralysis) ​ Pathway: Corticospinal tract Corticospinal Superior thalamic ○​ Sensory deficit to pain/temperature on right lower extremity Frontopontine Long Posterior limb radiation ​ Pathway: Spinothalamic tract Corticorubral ○​ Sensory deficit to proprioception on the left lower extremity Parieto pontine Posterior ​ Pathway: Dorsal Column Medial Lemniscus pathway Retrolenticular part Occipito pontine (optic) radiation ​ Location and Level of the Lesion: ○​ Right side of the spinal cord, at the level of T1 Inferior (auditory) Temporo pontine sublenticular part ​ This is an example of a Brown-Séquard lesion, a hemisection of radiation the spinal cord LIMBIC SYSTEM ​ Cingulate Gyrus ○​ Limited above by the cingulate sulcus ○​ Limited below by the corpus callosum ○​ Divided into Anterior Cingulate Cortex and Posterior Cingulate Cortex ​ Anterior Cingulate Cortex - involved in error and conflict detection ​ Posterior Cingulate Cortex - involved in the capacity to OS 202 Topic Name 6 of 8  C.​ CLINICAL INTERPRETATION ​ Neurofibromatosis type 2 ○​ A genetic condition that causes tumours to grow along your nerves ​ Hemicord lesion at a certain level of the spinal cord: ○​ Corticospinal tract: ipsilateral loss of motor function ○​ Dorsal column medial lemniscus pathway: ipsilateral proprioception deficit ○​ Spinothalamic tract: contralateral pain/temperature deficit OS 202 Topic Name 7 of 8  APPENDIX OS 202 Topic Name 8 of 8