Neurology II Flashcards
What is tegmental (Benedikt’s) Syndrome?
Due to lateral tegmental vascular infarct (in the midbrain)
Damage occurs to:
Red nucleus
Superior Cerebellar peduncle
Medial lemniscus
Spinothalamic tract
Oculomotor Nerve
Clinical deficits:
Cerebellar symptoms in contralateral limbs
(Intention tremor) – Red nuc.& Sup. Cer. peduncle
Contralateral loss of two-point tactile discrimination and loss of pain and thermal sense – Medial lemniscus & Spinothalamic tract
Ispilateral oculomotor nerve palsy – oculomotor nerve
What is superior alternating hemiplegia (Weber’s syndrome)?
Damage to ventral mesencephalon
**Damage occurs to (resulting in):** Corticospinal tract (contralateral hemiplegia)
Corticobulbar tract (contralateral hemiparesis of lower face)
Oculomotor nerve root fibers (Ipsilateral paralysis of oculomotor nerve)
What is Middle alternating hemiplegia?
Damage to the Ventral lower Pons
**Damage to (results in):** Corticospinal tract (contralateral hemiplegia)
Corticobulbar tract (Contralateral hemiparesis of lower face)
Abducens Nerve (Lower motor impairment of ipsilateral lateral rectus –> internal strabismus)
Millard-Gubler Syndrome
Damage to Ventral and Lateral pons
**Damage to (results in):** Corticospinal tract (contralateral hemiplegia)
Corticobulbar tract (contralateral hemiparesis of lower face)
Abducens nerve (lower motor impariment of ipsilateral lateral rectus –> internal strabismus)
Facial nerve (ipsilateral lower motor impairment of entire face)
Inferior alternating hemiplegia
Damage to ventral medulla
**Damage to (results in):** Corticospinal tract (contralateral hemiplegia)
Hypoglossal nerve (Lower motor impairment of ipsilateral tongue)
What are the brainstem CN reflexes?
Corneal reflex (CN V sensory –> CN VII Motor)
Pupillary Light Reflex (CN II sensory –> CN II motor)
Jaw Jerk Reflex (CN V sensory –> CN V motor)
Will basal ganglion lesions result in Upper or lower Motor neuron loss, or both?
Upper Motor Neuron only!
Although the basal ganglion controls amount of movement or how easy it is to make movements, it has no direct connection to lower motor neurons
What is the direct pathway through the basal ganglia?
Cerebral Cortex (all lobes) activate thespiny striatal neurons of the Striatum with Glutamate
Striatum (Caudate+Putamen) inhibits the Medial Palladial Segment (MPS) and Substantia Nigra pars reticularis (SNr) with GABA/Substance P
With MPS and SNr inhibited, they cannot inhibit the Thalamus (VA and VLa)
The Thalamus (VA and VLa) is then able to activate the Supplementary Motor Area (SMA) with Glutamate, thus facilitating movement
What is the indirect pathway of the basal ganglion?
Cerebral Cortex activates the spiny striatal neurons of the striatum with Glutamate
Striatum Inhibits the Lateral Palladial Segment (LPS) with GABA/Encephalin
The inhibited LPS then has decreased GABA release on the Subthalamic Nucleus (STN), thu disinhibiting it
The STN is then able to activate the MPS and SNr with Glutamate
Activated MPS and SNr inhibits the Thalamus (VA/VLa) with GABA
The inhibited Thalamus then has decreased Glutamate release onto the Supplementary Motor Area
And movement is suppressed
What are spiny neurons?
Efferent Neurons of the striatum
- Radiating dendrites w/spines
- Axons project to other Basal Ganglion nuclei
- Produce TWO DIFFERENT neurotransmitter combinations:
GABA/Substance P (Direct pathway)
GABA/Enkephalin (Indirect pathway)
What are aspiny neurons?
Local interneurons of Striatum
- Lack dendritic spines
- DO NOT project outside of striatum
- Produce many different NTs
(cholinergic ones most clinically important)
What are the affects of dopamine on the basal ganglion?
- directly activates spiny striatal neurons of direct pathway (to release GABA/Substance P)
- directly inhibits spiny striatal neurons of indirect pathway (to suppress release of GABA/Enkephalin)
- inhibits cholinergic aspiny striatal neurons that tonically activate spiny neurons of the indirect pathway (further inhibiting said pathway)
How does Parkinson’s disease affect the basal ganglion?
Substantia nigra pars compacta produces less and less dopamine resulting in:
Loss of dopaminergic input to basal ganglion
–> spiny neurons that release GABA/Substance P are less active
–> Spiny neurons that release GABA/Enkephalin are more activate
–> Hypokinetic disorder of parkinson’s:
Bradykinesia
Rigidity
Resting Tremor
Postural/Gait instability
Difficulty initiating movement
What is Huntington’s disease and how does it affect the basal ganglion?
Autosomal dominant hereditary neurodegenerative disease
- progressive degeneration of striatum (GABA/Enk neurons)
–> Loss of GABA/Enk neurons results in a decrease in indirect pathway activity, leading to a hyperkinetic disorder
Symptoms:
Chorea
Hypotonia
Psychiatric symptoms (depression, irritability, anxiety)
Cognitive decline
What is Hemiballism and what causes it?
Involuntary flinging of extremeties on contralateral side of the lesion
Results from a lesion (usually due to stroke) in the Subthalamic nucleus
Without the Subthalamic nucleus, the indirect pathway of the basal ganglion is unable to suppress unwanted movement through activation of the medial palladial segment and SNr (which would release GABA and inhibit the Thalamus)
–> without this pathway, the thalamus is constantly activated
What is the function of the thalamus?
- Receive all ascending sensory info (except olfaction)
- Receive systems concerned with motor activities
- Receive cerebellar output
- Receive the ARAS (maintain conciousness)
- Involved with the circuitry of limbic system
*No part of the cortex is without projections from the thalamus
What are the specific relay Thalamic nuclei that mediate motor activity?
Ventral Anterior
Ventral Lateral anterior (VLa)
Ventral Lateral posterior (VLp)
Dorsal Medial
What is Korsakoff’s Syndrome?
Vitamine B1 Thiamine Deficiency
(often assoc. w/alcoholism)
- Difficulty in acquiring new info
- Lack of insight
- Confabulation
- Apathy, in some cases, or talkative and repetitive behaviour in others
- Hallucinations
- Anterograde memory deficits
–> Treat w/Vitamine B1 injections
What is thalamic pain syndrome?
Burning, uncomfortable pain occuring after a cardiovascular acccident and affects the UE and face
Often involves intralaminar nuclei
Does not respond well to classical treatments
What is the pathway of the olfactory system?
Bipolar olfactory neurons receive input –> Connect with mitral cells in olfactory bulb/glomerulus –> Split info between Medial** and Lateral olfactory stria –> Amygdala + Olfactory Cortex (pyriform Ctx + Entorhinal Ctx) –> DM thalamic nucleus –> Orbitofrontal Ctx
** Medial olfactory stria make up the anterior commisure to connect olfactory tracts
What is Kallmann Syndrome?
Unable to smell: anosmia
–> due to small or absent olf. bulbs
- Failure of LHRH neuroblasts to enter olfactory bulb
- No LHRH neurons migrate to hypothalamus
- Pituitary gland does not produce LH and FSH
- Delayed puberty, sterility
What is the role of teh cingulate cortex in the limbic system?
- Coordinates intellect (cognition) and affect (emotions)
- Emotional processing through symbolic means (empahty, conflict resolution, decision making)
- Reduced actiity in schizophrenia
- Negative emotions in chornic pain syndromes
What is different about the structure of the hippocampal formation when compared to other cortexes of the brain?
The hippocamus only has 3 layers (vs 6 in other cortex)
–> thought to be due to lack of evolution (olfaction is oldest sense)
What is the function of the hippocampus? What is the pathway associated with that function?
It allows us to form new memories
Pathway:
Cortex –> Entorhinal Cortex –> Hippocampus
What kind of amnesia is caused by hippocampal lesions?
Anterograde Amnesia
(short term memory loss)
–> Declarative memory lost: unable to remember since time of lesion
–> Nondeclarative memory intact
What is the circuit for memory and emotional processing?
Papez circuit:
Cingulate Cortex –> via Cingulum to Hippocampus –> via Fornix to Mammillary Bodies –> via Mammillothalamic Tract to Anterior Thalamus –> via Internal Capsule to Cingulate cortex –> etc.
What is produced with stimulation of the septum? What is produced by a lesion of the septum?
Stimulation: Elicits pleasurable experience
–> Reward pathway of emotional processing
Lesion: Impaired learning – Perserevation (repetitive response)
What is the function of the amygdala?
- Label stimuli as negative or harmful
- Fear/anxiety response
- Stimulation results in: arrest response followed by fight or flight
What are the outputs of the amygdala after sensing danger?
Periaqueductal Gray Matter = pain suppression, analgesia
Autonomic Centers = hypyothalamus and brain stem tegmentum are activated (tachycardia, increased BP, respiration)
Reticular Formation = Vigilance/startle
Paraventricular Nucleus = Corticotrphin Releasing Hormone (stress hormone)
Dorsal Medial Thalamic nuclei = Planning & judgement
What is produced by damage to the amygdala in animals?
Kluver-Bucy Syndrome:
- Tameness: loss of emotional responsiveness
- Psychic blindness: unable to recognize the meaning of objects by sight
- Hyperoral and hypersexual responses
What is produced by damage to the amygdala in humans?
Urbach-Wieth Syndrome:
- Genetic disorder
- Bilateral calcification of amygdala
- Unable to “read” emotions of others
- Tend to have less fear of danger
