Neuro Flashcards
Temporal, parietal lobe VF defect
mnemonic PITS (parietal-inferior, temporal-superior) Mnemonics: temporal lobe = pie in the sky. Parietal lobe = pie on the floor.
But everybody, you can figure out the answer if you just realize that the nerve fibers exit the eye in the same orientation they were in the retina. I.e. superior retina => nerve fibers in the upper half of the nerve => nerve fibers going to the upper optic radiations (parietal lobe is above temporal lobe).
temporal lobe = pie in the sky. Parietal lobe = pie on the floor.
Of course the retina has an inverted image projected onto it, so the INFERIOR visual field is seen by the superior retina.
So therefore, the parietal lobe optic radiations carry the vision of the inferior hemi-field.
Visual information for the left side of the visual field in both eyes exits the optic chiasm and synapses in the right lateral geniculate nucleus. This information then passes from the right lateral geniculate nucleus to the right primary visual area of the occipital lobe (Brodmann area 17) by way of the optic radiations. Visual information (in the optic radiations) which correspond to the left superior quadrant of the visual field in both eyes passes through the right temporal lobe in a pathway called the loop of Meyer. Meanwhile, visual information (in the optic radiations) for the left inferior quadrant of the visual field in both eyes passes through the parietal lobe. The clinical significance of this complicated pathway is that a lesion of the right temporal lobe results in loss of the left superior quadrant of the visual field in both eyes (also known as a left homonymous superior quadrantanopia).
Palinopsia
Think of Sarah PALIN and how she kept popping back up (recurring) even after losing the race (i.e. Being removed from the field)
PalinOpsia most common cause is lesion in Parietal-Occiptal region
Palinopsia is a phenomenon marked by the persistence or recurrence of images following removal of the stimulus from the visual field. The most common cause is a lesion of the parieto-occipital region (usually the non-dominant, right side of brain) with an associated contralateral hemi-field visual field defect.
In this instance, the phenomenon usually occurs within the blind portion of the visual field. Also associated are topiramate, clomiphene, trazodone, and prior use of hallucinogenic drugs (especially LSD and mushrooms). Episodic migraine associated palinopsia has been described as well.
There are isolated reports of palinopsia related to epileptiform activity in the parieto-occipital region although most neuro-ophthalmologists do not believe that palinopsia in most cases is a seizure-related phenomenon.
Optic nerve edema
6 Ms meaty (pseudotumor) mass (tumor) medication (amiodarone, accutane, tetracyclines) meningitis MS malignant HTN
CN 3 palsy syndromes
CLUMSY: Claude (ataxia)
WEAK: Weber (hemiparesis)
BLOODY: Benedikt (blood is red like red nucleus)
BENEDICT Arnold was a general for the continental army during the revolutionary war who defected to the CONTRALATERAL SIDE and became a RED coat. He was scared after doing so and always had a TREMOR.
Benedikt syndrome: 2/2 midbrain lesion affecting the 3rd nerve fascicle and the red nucleus which causes an ipsilateral 3rd nerve palsy and a contralateral “rubral” tremor (a slow tremor present with activity and rest).
Weber syndrome is the 3rd nerve correlate of Raymond syndrome: 2/2 midbrain lesion causing a fascicular 3rd nerve palsy and a contralateral hemiparesis.
Claude syndrome: 2/2 damage to the dorsal midbrain affecting the superior cerebellar peduncle and 3rd nerve fasciculus typically resulting in ipsilateral 3rd nerve palsy and contralateral ataxia.
mnemonic: rayMOND = Mid PONS (so CN6) Weber: caught in the MIDDLE of the WEB (midbrain, so CN3) Red Benedikt (rhymes with eggs benedict): Red Traiter TREMBLES (RUBRAL tremor from RED nucleus)
Clumsy Claude Cerebellum (Ataxia from superior cerebellar peduncle); Just remember that all are CN3 except RayMOND (cuz its down in the Mid-PONS!)
Raymond
rayMOND = Mid PONS (so CN6)
Raymond syndrome is a 6th nerve palsy with a contralateral hemiparesis due to a lesion in the mid-pons affecting the 6th nerve fasciculus along with the corticospinal tract.
Marcus Gunn jaw winking
If you’re an OPEN (mouth) person, you focus EXTERNALLY (external pterygoid)
If you’re a CLOSED (mouth) person, you focus INTERNALLY (internal pterygoid)
Marcus Gunn jaw-winking syndrome is a synkinetic phenomena caused by congenital “miswiring” of the innervation to the levator palpebrae superioris.
Marcus Gunn jaw-winking syndrome is a variant of congenital ptosis with fibrosis and poor function of the levator palpebrae superioris. If the affected ptotic upper eyelid elevates upon opening of the mouth, movement of the mandible to the contralateral side, or jaw protrusion then there are aberrant connections between the external pterygoid muscle and the levator palpebrae superioris leading to synkinetic movements.
If the affected ptotic upper eyelid elevates upon closure of the mouth, then there are aberrant connections between the internal pterygoid muscle and the levator palpebrae superioris leading to synkinetic movments.
CN4 palsy
GOTS: Gaze Opposite, Tilt Same (makes diplopia worse)
Right IVth worse on Right head turn (left gaze) and right head tilt
Melkersson-Rosenthal syndrome (MRS) syndrome
Memory tool: Tongue looks funny from drinking “Melk.”
-associated with CN VII palsy
-characterized by the clinical triad of recurrent facial paralysis (~30% of cases), orofacial edema (usually the lips; “cheilitis”), and lingua plicata (i.e. fissured tongue). A lip biopsy can be helpful in the diagnosis of MRS and would demonstrate a typical granulomatous infiltration.
As of 2011, the exact cause of MRS is not known and there is no well-defined treatment for this disorder. Some clinicians will inject corticosteroid to reduce the lip swelling. Others have tried a wide variety of immunomodulatory agents to suppress the swelling episodes.
Millard Guber
It is caused by a lesion in the ventral pons that disrupts: 1) the 6th nerve fasciculus resulting in an ipsilateral abduction deficit; 2) the corticospinal tract before decussation in the medulla causing contralateral spastic hemiplegia; and 3) the 7th nerve fasciculus resulting in an ipsilateral facial weakness.
One way to remember what is affected is to count the letters in Millard (7) and Gubler (6) . The syndrome affects the 6th and 7th nerve……
Blepharospasm and hemifacial spasm
HemiFACIAL spasm= 7thn (FACIAL n) affected secondary to vascular compression, ONE side affected (HEMI) ; Tx Botox
Blepharospasm=Bilateral= Basal ganglia dysfunction= Blocked by sleep(stops with sleep) Tx: Botox
CAR vs MAR
CAR = “C”ones “A”nd “R”ods; MAR = “M”ostly “A”ffects “R”ods
Kearns Sayre
Kearns-Sayre triad: Eyes cant track, retinas black, heart attack.
classic clinical findings of Kearns-Sayre syndrome: chronic progressive external ophthalmoplegia (CPEO), retinal pigmentary changes, and cardiomyopathy. An EKG is necessary to diagnose the presence of possible heart block.
full differential diagnosis for paradoxical pupillary reaction
Mnemonic : paraphrase the word Paradoxical to Baradoxical : B : Bests A : achromatopsia R : RP A : Albinism D : dominant optic atrophy O : ONH XI : none C : CSNB L : Lebers
Early onset (usually congenital) disease of optic nerve or retinal disease can result in a paradoxical pupillary reaction. Affected patients will have immediate pupillary constriction instead of dilation upon turning the exam room lights off.
The finding is most significant clinically in young children with poor vision of unknown etiology. Paradoxical pupillary reaction is highly suggestive of optic nerve or retinal pathology.
Leber’s hereditary ON
To remember 11778: I ate(8) at the 7-11 twice.
From: Mutations in mitochondrial DNA, usually at position 11778. The rate of spontaneous late visual recovery in the 14484 mutation is about 65% as opposed to only 4% in the more common 11778 mutation.
14484… = LAATE visual recovery (1=L, 4=A, 8=ate)
11778=HeLL (almost nobody escapes when they are in that mutation)
MC nucleotide deletion position of Lebers is 11778. Leads to an abnormality in the NADH dehydrogenase of the mitochondria.
Manifests in males aged 10-30 years old. It presents as an acute, severe (<20/200), painless, monocular visual loss with central scotoma.
3 findings that are classic: 1) elevation of the disc; 2) peripapillary telangiectasia; and 3) retinal arteriolar tortuosity. The second optic nerve becomes involved weeks to months later.
Tonic slow muscle fibers
Felderstruktur
F’elder’strukter: old people are slower and enjoy wine tasting (en grappe [grapes])
