Thank you, I'm learning a lot from these lectures! Timestamps for revision: 0:20 Pathways, 3:14 hemisection of the spinal cord / tracts, 15:56 diagram 1:15 Posterior collumns: sacral fibers medially, corticospinal + spinothalamic tracts: sacral laterally. Example 48:42 2:15 Thoracic cord: small ventral horns, distinctive intermediolateral cell collumn (preganglionic sympathetic fibers), clark's nucleus (relay nucleus for dorsal spinocerebellar tract), substantia gelatinosa (synapse/pain/temp). 4:19 Spinal cord disease categories 5:01 *Compressive myelopathy* causes, PbKTL, 7:56 *Spondylosis and disk herniation* , radicular symptoms at the level of the lesion, Lhermitte's: posterior collumns 11:13 *Brown Sequard syndrome* 12:05 Superficial abdominal reflexes, (unlike deep tendon reflexes, they move all the way up to the brain, absent in a lot of normal individuals) 14:16 *Autonomic dysreflexia* - unregulated sympathetic overactivation (lesions above T6, >1 month), triggers eg bladder distention, catheter change. Watch out for BP elevation. 16:57 *Acute spinal cord trauma* , high dose steroids, neurosurgery 18:41 *Transverse myelitis* , non-traumatic, MS most common cause. UMN findings but consider spinal cord shock. 21:08 Tight band sensation due to disruption of pain and temp fibers at that level 21:29 *AIDS myelopathy* , 20% 21:52 *Anterior spinal artery occlusion* : not posterior columns, thoracic artery surgery - art. of Adamkiewicz (also 22:44, supplies lower up to the mid thoracic cord, there's a watershed area just above) 23:54 Treatment of spasticity: baclofen (spinal cord GABA-A rec +), diazepam, botulinum toxin 26:09 Prominent LMN findings: *polio* , anterior horn cells (ocasionally the lower motor neurons in the medulla can be affected). 29:31 *West Nile virus* , up to 2 weeks incubation, severe (neurologic) involvement less than 1%, encephalitis, meningitis, acute flaccid paralysis. IgM serum, CSF. 34:58 Corticobulbar tract 32:39 *ALS* = UMN + LMN lesions. UMN due to corticospinal + corticobulbar *tract* degeneration (pseudobulbar palsy: lesion of the motor neurons that are in the cortex, which in turn degenerates (38:16 + 38:43 MRI, Wallerian degeneration) the pathway supplying the bulb = lesion not in the bulb itself. Dysarthria, dysphagia, emotional incontinence. LMN due to anterior horn cell degeneration (35:18): bulbar palsy (dysarthria, dysphagia + tongue atrophy, no emotional incontinence). 36:51 onset of symptoms in ALS, 20% start with dysarthria or dysphagia and have a worse prognosis, especially if bulbar (42:22). 37:15 What is preserved in ALS, Onuf's nucleus (anterior horn cells S2-4) is preserved: bowel and bladder control preserved. 38:58 ALS age of onset, incidence, sporadic, familial. 39:55 Genetics: Superoxide dismutase, *C9orf72* , TDP-43. Frontotemporal dimentia in 10% of ALS patients. 42:42 Motor neuron disease is a spectrum disorder that can sometimes include pure LMN involvement throughout the course (progressive muscular atrophy) or pure UMN involvement (primary lateral sclerosis). 43:32 *Riluzole* (blocks the effects of NMDA?) extends life 2-3 months. Edaravone? 45:13 Conditions that mainly affect sensory pathways in the spinal cord. 45:18 *Syringomyelia* , trauma, Arnold Chiari type I malformations (45:50 low line cerebellar tonsils, central cavity) 46:42 pain + temp, bilateral, *syringobulbia* , 48:02 + *UMN* 48:17 *Intramedullary tumors* , ependymomas, astrocytomas, start centrally, expand towards spinothalamic tracts, sacral dermatomes may be spared. 49:18 *B12 deficiency* : gait instability (most common presentation: dysfunction of posterior columns), corticospinal (UMN findings?) + pain/temperature also affected (stock & gloves), 51:10 MRI degeneration of posterior column. 51:30 other neurologic presentations. Methylmalonic acid (more sensitive for detecting symptomatic B12 deficiency) & homocysteine levels. 53:42 *Tabes dorsalis* , HIV, sensory roots affected, radicular painful symptoms. 54:17 *Posterior spinal artery occlusion* , posterior spinal artery, not common, posterior columns 54:07 *Friedreich's ataxia* , AR, spinocerebellar pathways, peripheral neuropathy (sensory ataxia), posterior columns, corticospinal tract (spasticity). Rapidly progressive instability. Diagnosis 3nucleotide GAA repeat (X9). Friedreich's, myotonic dystrophy and Huntington's are 3nucleotide repeat disorders. 🟡🟡 *BLADDER CONTROL* 🟡🟡 56:43 *Bladder anatomy* _Pelvic nerve: sensory input about bladder fullness+parasympathetic fibers to stimulate the detrusor muscle (ACH, M3), Hypogastric nerve: sympathetic fibers (NA, β3, α1) to inhibit detrusor and contract internal ur. sphincter. Pudendal nerve: somatic fibers (ACH, nic) to the external urethral sphincter/EUS_ *Basically: sympathetic: prevents voiding, parasympathetic: stimulates voiding, somatic motor system: voluntary control* 57:16 *NORMAL FILLING OF THE BLADDER* : Mechanoreceprors activate the pelvic nerve (S2-4 roots) which in turn: a) (+)symp. neurons: they supply the bladder via the hypogastric nerve to inhibit voiding via 2 mechanisms (contraction of IUS, inhibition of the detrusor=εξωστήρας). b) (+) Onuf's nucleus (anterior horn of S2) , somatic motor neurons that travel with the pudendal nerve - *voluntary control* : external urethral sphincter is kept closed up. 58:26 Info for normal filling also travels higher up: periaquedactal grey PAG, prefrontal cortex (PFC)/paracentral lobule. 59:13 *NORMAL VOIDING OF THE BLADDER* : PFC activates PAG which activates the pontine micturition center PMC (switch): inhibition of symp. and Onuf's nucleus (pudendal nucleus), activation of parasymp. 1:00:52 *Neurotransmitters* Parasymp: pelvic nerve, ACH: (+) M3 rec to activate the detrusor m. Symp: hypogastric nerve, NA: (-) β3 rec to inhibit the detrusor & (+) α1 rec to contract internal urethral sphingter. Females: no internal ur. sphincter. Onuf's nucleus, pudendal nerve, ACH/nicotinic rec to contract external urethral sphincter. *Pathology* 1:02:27 Bilateral medial frontal lobe lesion, 1:03:23 Spinal cord compression, oxybutynin blocks M rec to relax detrusor, PVR = post void residual, 1:05:55 Lower motor neuron lesion S2-4 can affect Onuf's output and parasympathetic outflow to the bladder > flaccid bladder > overflow incontinence
@@bacolive I just type the timestamp as I see it in the video and youtube does the rest (the timestamps turn blue once I post my comment). As an uploader, you can add "chapters" to your videos by typing timestamps in your *video description* instead of in the comment section. Just make sure your first timestamp is 0:00 and that at least 2 chapters follow, like so: 0:00 Intro 5:01 Compressive myelopathy 7:56 Spondylosis and disk herniation I've taken some liberties with my comment, however timestamps have to be in *ascending order* for chapters to be added. Once you hit "save", not only will your video description look similar to my comment but youtube will also incorporate the chapter titles in the progress bar of your video.
This lecture taught me a lot, even new things I haven’t heard elsewhere like upper motor neuron lesion signs in same side as lesion. So if you had upper motor findings on both sides would that point to motor cortex?
Doctor I have an urgent question, and I hope you are available to reply. You have mentioned that there are few causes of mixed UMN and LMN lesions like ALS and spondylosis. Yet I have a question regarding any lesion that takes a great segment of the spinal cord for example transverse myelitis or brown sequard. Isn't it supposedly to cause both UMN and LMN lesion since both the descending corticospinal tracts, and the AHC are affected. I hope you clarify this point.
Thank you, I'm learning a lot from these lectures!
Timestamps for revision:
0:20 Pathways, 3:14 hemisection of the spinal cord / tracts, 15:56 diagram
1:15 Posterior collumns: sacral fibers medially, corticospinal + spinothalamic tracts: sacral laterally. Example 48:42
2:15 Thoracic cord: small ventral horns, distinctive intermediolateral cell collumn (preganglionic sympathetic fibers), clark's nucleus (relay nucleus for dorsal spinocerebellar tract), substantia gelatinosa (synapse/pain/temp).
4:19 Spinal cord disease categories
5:01 *Compressive myelopathy* causes, PbKTL, 7:56 *Spondylosis and disk herniation* , radicular symptoms at the level of the lesion, Lhermitte's: posterior collumns
11:13 *Brown Sequard syndrome*
12:05 Superficial abdominal reflexes, (unlike deep tendon reflexes, they move all the way up to the brain, absent in a lot of normal individuals)
14:16 *Autonomic dysreflexia* - unregulated sympathetic overactivation (lesions above T6, >1 month), triggers eg bladder distention, catheter change. Watch out for BP elevation.
16:57 *Acute spinal cord trauma* , high dose steroids, neurosurgery
18:41 *Transverse myelitis* , non-traumatic, MS most common cause. UMN findings but consider spinal cord shock.
21:08 Tight band sensation due to disruption of pain and temp fibers at that level
21:29 *AIDS myelopathy* , 20%
21:52 *Anterior spinal artery occlusion* : not posterior columns, thoracic artery surgery - art. of Adamkiewicz (also 22:44, supplies lower up to the mid thoracic cord, there's a watershed area just above)
23:54 Treatment of spasticity: baclofen (spinal cord GABA-A rec +), diazepam, botulinum toxin
26:09 Prominent LMN findings: *polio* , anterior horn cells (ocasionally the lower motor neurons in the medulla can be affected).
29:31 *West Nile virus* , up to 2 weeks incubation, severe (neurologic) involvement less than 1%, encephalitis, meningitis, acute flaccid paralysis. IgM serum, CSF.
34:58 Corticobulbar tract
32:39 *ALS* = UMN + LMN lesions.
UMN due to corticospinal + corticobulbar *tract* degeneration (pseudobulbar palsy: lesion of the motor neurons that are in the cortex, which in turn degenerates (38:16 + 38:43 MRI, Wallerian degeneration) the pathway supplying the bulb = lesion not in the bulb itself. Dysarthria, dysphagia, emotional incontinence.
LMN due to anterior horn cell degeneration (35:18): bulbar palsy (dysarthria, dysphagia + tongue atrophy, no emotional incontinence).
36:51 onset of symptoms in ALS, 20% start with dysarthria or dysphagia and have a worse prognosis, especially if bulbar (42:22).
37:15 What is preserved in ALS, Onuf's nucleus (anterior horn cells S2-4) is preserved: bowel and bladder control preserved.
38:58 ALS age of onset, incidence, sporadic, familial.
39:55 Genetics: Superoxide dismutase, *C9orf72* , TDP-43. Frontotemporal dimentia in 10% of ALS patients.
42:42 Motor neuron disease is a spectrum disorder that can sometimes include pure LMN involvement throughout the course (progressive muscular atrophy) or pure UMN involvement (primary lateral sclerosis).
43:32 *Riluzole* (blocks the effects of NMDA?) extends life 2-3 months. Edaravone?
45:13 Conditions that mainly affect sensory pathways in the spinal cord.
45:18 *Syringomyelia* , trauma, Arnold Chiari type I malformations (45:50 low line cerebellar tonsils, central cavity) 46:42 pain + temp, bilateral, *syringobulbia* , 48:02 + *UMN*
48:17 *Intramedullary tumors* , ependymomas, astrocytomas, start centrally, expand towards spinothalamic tracts, sacral dermatomes may be spared.
49:18 *B12 deficiency* : gait instability (most common presentation: dysfunction of posterior columns), corticospinal (UMN findings?) + pain/temperature also affected (stock & gloves), 51:10 MRI degeneration of posterior column. 51:30 other neurologic presentations. Methylmalonic acid (more sensitive for detecting symptomatic B12 deficiency) & homocysteine levels.
53:42 *Tabes dorsalis* , HIV, sensory roots affected, radicular painful symptoms.
54:17 *Posterior spinal artery occlusion* , posterior spinal artery, not common, posterior columns
54:07 *Friedreich's ataxia* , AR, spinocerebellar pathways, peripheral neuropathy (sensory ataxia), posterior columns, corticospinal tract (spasticity). Rapidly progressive instability. Diagnosis 3nucleotide GAA repeat (X9). Friedreich's, myotonic dystrophy and Huntington's are 3nucleotide repeat disorders.
🟡🟡 *BLADDER CONTROL* 🟡🟡
56:43 *Bladder anatomy*
_Pelvic nerve: sensory input about bladder fullness+parasympathetic fibers to stimulate the detrusor muscle (ACH, M3), Hypogastric nerve: sympathetic fibers (NA, β3, α1) to inhibit detrusor and contract internal ur. sphincter. Pudendal nerve: somatic fibers (ACH, nic) to the external urethral sphincter/EUS_ *Basically: sympathetic: prevents voiding, parasympathetic: stimulates voiding, somatic motor system: voluntary control*
57:16 *NORMAL FILLING OF THE BLADDER* : Mechanoreceprors activate the pelvic nerve (S2-4 roots) which in turn:
a) (+)symp. neurons: they supply the bladder via the hypogastric nerve to inhibit voiding via 2 mechanisms (contraction of IUS, inhibition of the detrusor=εξωστήρας).
b) (+) Onuf's nucleus (anterior horn of S2) , somatic motor neurons that travel with the pudendal nerve - *voluntary control* : external urethral sphincter is kept closed up. 58:26 Info for normal filling also travels higher up: periaquedactal grey PAG, prefrontal cortex (PFC)/paracentral lobule.
59:13 *NORMAL VOIDING OF THE BLADDER* :
PFC activates PAG which activates the pontine micturition center PMC (switch): inhibition of symp. and Onuf's nucleus (pudendal nucleus), activation of parasymp.
1:00:52 *Neurotransmitters*
Parasymp: pelvic nerve, ACH: (+) M3 rec to activate the detrusor m.
Symp: hypogastric nerve, NA: (-) β3 rec to inhibit the detrusor & (+) α1 rec to contract internal urethral sphingter. Females: no internal ur. sphincter.
Onuf's nucleus, pudendal nerve, ACH/nicotinic rec to contract external urethral sphincter.
*Pathology*
1:02:27 Bilateral medial frontal lobe lesion, 1:03:23 Spinal cord compression, oxybutynin blocks M rec to relax detrusor, PVR = post void residual, 1:05:55 Lower motor neuron lesion S2-4 can affect Onuf's output and parasympathetic outflow to the bladder > flaccid bladder > overflow incontinence
That's awesome! How do you do that?
@@bacolive I just type the timestamp as I see it in the video and youtube does the rest (the timestamps turn blue once I post my comment).
As an uploader, you can add "chapters" to your videos by typing timestamps in your *video description* instead of in the comment section. Just make sure your first timestamp is 0:00 and that at least 2 chapters follow, like so:
0:00 Intro
5:01 Compressive myelopathy
7:56 Spondylosis and disk herniation
I've taken some liberties with my comment, however timestamps have to be in *ascending order* for chapters to be added.
Once you hit "save", not only will your video description look similar to my comment but youtube will also incorporate the chapter titles in the progress bar of your video.
@@ranialian8537 Thanks so much!!
Are there recorderd lectures for Dr.Deicher? Also, great lecture as always really learn a lot watching them appreciated u uploading them
Thanks for the lecture sir !! 🙏
This lecture taught me a lot, even new things I haven’t heard elsewhere like upper motor neuron lesion signs in same side as lesion. So if you had upper motor findings on both sides would that point to motor cortex?
Doctor I have an urgent question, and I hope you are available to reply. You have mentioned that there are few causes of mixed UMN and LMN lesions like ALS and spondylosis. Yet I have a question regarding any lesion that takes a great segment of the spinal cord for example transverse myelitis or brown sequard. Isn't it supposedly to cause both UMN and LMN lesion since both the descending corticospinal tracts, and the AHC are affected. I hope you clarify this point.