{"id":1533,"date":"2023-12-24T14:11:36","date_gmt":"2023-12-24T22:11:36","guid":{"rendered":"https:\/\/alteritas.net\/alteritas\/?p=1533"},"modified":"2023-12-24T15:03:35","modified_gmt":"2023-12-24T23:03:35","slug":"highlight-notes-from-neurology-readings","status":"publish","type":"post","link":"https:\/\/alteritas.net\/alteritas\/2023\/12\/24\/highlight-notes-from-neurology-readings\/","title":{"rendered":"Highlight Notes \/ The Only Neurology Book You’ll Ever Need"},"content":{"rendered":"

Notebook Export<\/span><\/p>\n

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The Only Neurology Book You’ll Ever Need<\/div>\n
Thaler, Alison I.; Thaler, Malcolm S.<\/div>\n
Citation (MLA): Thaler, Alison I., and Malcolm S. Thaler. The Only Neurology Book You’ll Ever Need<\/i>. Wolters Kluwer Health, 2021. Kindle file.<\/div>\n
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Chapter 1 Let\u2019s Get Started: Your Neurologic Toolbox<\/div>\n
Highlight(blue<\/span>) – CASE 1 > Page 23 \u00b7 Location 337<\/div>\n
In a broad sense, all disease is experienced through the nervous system.<\/div>\n
Highlight(blue<\/span>) – CASE 1 > Page 24 \u00b7 Location 340<\/div>\n
It\u2019s all in your head, whether it\u2019s mental confusion or a skinned knee.<\/div>\n
Highlight(blue<\/span>) – Neuroanatomy: The Basics > Page 25 \u00b7 Location 360<\/div>\n
communicate, whereas<\/div>\n
Highlight(blue<\/span>) – Electrophysiology in Two Pages > Page 36 \u00b7 Location 427<\/div>\n
There are many types of neurotransmitters; most of the ones you know already are small peptides such as acetylcholine, GABA, glutamate, serotonin, and the catecholamines (dopamine, epinephrine, and norepinephrine).<\/div>\n
Highlight(blue<\/span>) – Mental Status > Page 49 \u00b7 Location 544<\/div>\n
\u201capraxic.\u201d<\/div>\n
Highlight(blue<\/span>) – Cranial Nerves > Page 53 \u00b7 Location 574<\/div>\n
Nasolabial fold flattening<\/div>\n
Highlight(blue<\/span>) – The Motor System > Page 55 \u00b7 Location 589<\/div>\n
They decussate (or cross) in the medulla at the medullary pyramids, right where the brainstem meets the spinal cord;<\/div>\n
Highlight(blue<\/span>) – The Motor System > Page 57 \u00b7 Location 605<\/div>\n
extrapyramidal system, runs outside the medullary pyramids (hence extrapyramidal) and includes neurons within the basal ganglia and cerebellum, among other locations. Unlike the neurons of the pyramidal system, these neurons synapse all over the place and are important for indirect, largely involuntary, modulation, coordination, and regulation of movements.<\/div>\n
Highlight(blue<\/span>) – The Motor System > Page 58 \u00b7 Location 608<\/div>\n
Dopamine depletion within the basal ganglia, for instance, as in Parkinson disease, can result in tremor and bradykinesia (slowness of movement).<\/div>\n
Highlight(blue<\/span>) – The Motor System > Page 62 \u00b7 Location 634<\/div>\n
Extrapyramidal dysfunction is responsible for many of the manifestations of Parkinson disease, including tremor, abnormal posture, and gait dysfunction.<\/div>\n
Highlight(blue<\/span>) – The Motor System > Page 62 \u00b7 Location 647<\/div>\n
\u201cconfrontation testing.\u201d<\/div>\n
Highlight(blue<\/span>) – The Somatosensory System > Page 69 \u00b7 Location 703<\/div>\n
eyes closed, patients can only rely on proprioception, so if proprioception is impaired, they will lose their balance.<\/div>\n
Highlight(blue<\/span>) – Coordination > Page 76 \u00b7 Location 745<\/div>\n
dysmetria.<\/div>\n
Highlight(blue<\/span>) – Gait > Page 78 \u00b7 Location 759<\/div>\n
Ataxic gait.<\/div>\n
Highlight(blue<\/span>) – Gait > Page 78 \u00b7 Location 761<\/div>\n
Shuffling gait.<\/div>\n
Highlight(blue<\/span>) – Gait > Page 78 \u00b7 Location 761<\/div>\n
Classic for Parkinson disease, this type of gait can also be seen in normal pressure hydrocephalus. It is characterized by small short steps with very little foot elevation off the ground.<\/div>\n
Highlight(blue<\/span>) – Is it Neurologic? > Page 82 \u00b7 Location 812<\/div>\n
where, anatomically, they come from (or, in neurologist speak, \u201clocalize to\u201d).<\/div>\n
Highlight(blue<\/span>) – Diagnostic Tools > Page 86 \u00b7 Location 849<\/div>\n
LP, EEG, and EMG\/ NCS\u2014form the crux of the diagnostic toolbox for neurologic disease.<\/div>\n
Highlight(blue<\/span>) – A Quick Overview of Head Imaging > Page 88 \u00b7 Location 879<\/div>\n
Radiologists use the term \u201cintensity\u201d as opposed to \u201cdensity\u201d to describe brightness on an MRI: things that appear bright are referred to as \u201chyperintense\u201d (or \u201cincreased signal\u201d), and things that appear dark are \u201chypointense\u201d (or \u201cdecreased signal\u201d).<\/div>\n
Chapter 2 Stroke and Cerebrovascular Disease<\/div>\n
Bookmark – Page 108 \u00b7 Location 1036<\/div>\n
Highlight(blue<\/span>) – Cerebrovascular Anatomy > Page 117 \u00b7 Location 1107<\/div>\n
this is why posterior communicating artery aneurysms can cause third nerve palsies!<\/div>\n
Chapter 3 Headache<\/div>\n
Highlight(blue<\/span>) – Migraine > Page 209 \u00b7 Location 2026<\/div>\n
cytokines.<\/div>\n
Highlight(blue<\/span>) – Trigeminal Autonomic Cephalalgias (TACs) > Page 220 \u00b7 Location 2142<\/div>\n
Trigeminal Autonomic Cephalalgias (TACs)<\/div>\n
Highlight(blue<\/span>) – Trigeminal Autonomic Cephalalgias (TACs) > Page 221 \u00b7 Location 2148<\/div>\n
Trigeminal nerve distributions: V1 (ophthalmic), V2 (maxillary), V3 (mandibular).<\/div>\n
Highlight(blue<\/span>) – Trigeminal Autonomic Cephalalgias (TACs) > Page 221 \u00b7 Location 2151<\/div>\n
SUNCT (short-lasting unilateral neuralgiform headache with conjunctival injection and tearing) and SUNA (short-lasting unilateral neuralgiform headache with autonomic symptoms).<\/div>\n
Highlight(blue<\/span>) – Trigeminal Autonomic Cephalalgias (TACs) > Page 222 \u00b7 Location 2153<\/div>\n
These headaches are characterized by sudden attacks of stabbing, unilateral pain that last only a few seconds but can occur hundreds of times a day. The attacks are often triggered by tactile or cutaneous stimuli, such as bathing, brushing one\u2019s hair, or shaving. SUNCT presents with both conjunctival injection and tearing;<\/div>\n
Highlight(blue<\/span>) – Trigeminal Autonomic Cephalalgias (TACs) > Page 222 \u00b7 Location 2157<\/div>\n
Lamotrigine<\/div>\n
Highlight(blue<\/span>) – Trigeminal Autonomic Cephalalgias (TACs) > Page 223 \u00b7 Location 2183<\/div>\n
Preventive Treatment Lamotrigine Indomethacin Verapamil, Galcanezumab Indomethacin<\/div>\n
Highlight(blue<\/span>) – Sinus Headache > Page 224 \u00b7 Location 2196<\/div>\n
diagnosis, in reality very few headaches are directly associated with acute or chronic sinusitis.<\/div>\n
Highlight(blue<\/span>) – Sinus Headache > Page 225 \u00b7 Location 2202<\/div>\n
Pain around the sinuses, without evidence of an upper respiratory infection, is rarely a sinus headache, but far more often a manifestation of migraine.<\/div>\n
Bookmark – Neuralgias > Page 226 \u00b7 Location 2207<\/div>\n
Highlight(blue<\/span>) – Neuralgias > Page 226 \u00b7 Location 2208<\/div>\n
Trigeminal Neuralgia<\/div>\n
Highlight(blue<\/span>) – Neuralgias > Page 226 \u00b7 Location 2208<\/div>\n
(TN), TN presents with unilateral, brief episodes of shock-like pain that occur in the distribution of one or more divisions of the trigeminal nerve; the maxillary and mandibular branches (V2 and V3) are more commonly affected than the ophthalmic division (V1).<\/div>\n
Highlight(blue<\/span>) – Neuralgias > Page 227 \u00b7 Location 2213<\/div>\n
Classical TN. Classical TN is due to neurovascular compression causing morphological changes in the trigeminal nerve root. An abnormal vascular loop compresses the trigeminal nerve around its dorsal<\/div>\n
Highlight(blue<\/span>) – Neuralgias > Page 227 \u00b7 Location 2215<\/div>\n
Secondary TN.<\/div>\n
Highlight(blue<\/span>) – Neuralgias > Page 227 \u00b7 Location 2215<\/div>\n
This refers to TN caused by an underlying disease,<\/div>\n
Highlight(blue<\/span>) – Neuralgias > Page 227 \u00b7 Location 2222<\/div>\n
Carbamazepine and oxcarbazepine are commonly used treatments for classical and idiopathic TN.<\/div>\n
Highlight(blue<\/span>) – Neuralgias > Page 227 \u00b7 Location 2224<\/div>\n
gabapentin<\/div>\n
Chapter 7 Neurocognitive Disorders and Dementia<\/div>\n
Highlight(blue<\/span>) – Cognitive Impairment > Page 364 \u00b7 Location 3565<\/div>\n
Fifteen percent of patients with MCI over the age of 65 will go on to develop overt dementia within 2 years; this statistic can unnerve even the most stoical among your patients, so remember to emphasize to them that this means that 85% of people with MCI will not progress to dementia during that period.<\/div>\n
Highlight(blue<\/span>) – Alzheimer Disease (AD) > Page 368 \u00b7 Location 3614<\/div>\n
allele.<\/div>\n
Chapter 13 Parkinson Disease and Other Movement Disorders<\/div>\n
Highlight(blue<\/span>) – Etiology > Page 656 \u00b7 Location 6215<\/div>\n
The pathology involves the loss of primarily dopaminergic neurons within the substantia nigra (a part of the basal ganglia located in the midbrain), as well as the destruction of neurons, both dopaminergic and otherwise, in other areas of the brain.<\/div>\n
Highlight(blue<\/span>) – Clinical Presentation > Page 658 \u00b7 Location 6225<\/div>\n
PD causes four classic physical signs that are the result of involvement of the extrapyramidal motor system, the part of the motor system involved in modulation and regulation of movement:<\/div>\n
Highlight(blue<\/span>) – Clinical Presentation > Page 658 \u00b7 Location 6229<\/div>\n
akinesia for the often more accurate bradykinesia).<\/div>\n
Highlight(blue<\/span>) – Clinical Presentation > Page 659 \u00b7 Location 6233<\/div>\n
The extrapyramidal system is everything else that impacts movement, and includes neurons within the basal ganglia and cerebellum. In general, the pyramidal system causes voluntary movement, whereas the extrapyramidal system causes involuntary movement, indirectly regulating and modulating the activity of the pyramidal system. See page 18 for a more comprehensive review of motor system anatomy.<\/div>\n
Highlight(blue<\/span>) – Clinical Presentation > Page 659 \u00b7 Location 6239<\/div>\n
unilaterally and then spreads contralaterally over a course of months to years.<\/div>\n
Highlight(blue<\/span>) – Clinical Presentation > Page 661 \u00b7 Location 6252<\/div>\n
To be clear, though, don\u2019t be confused by the seemingly contradictory prefixes: although the rigidity associated with PD is a form of hypertonia, PD itself is a hypokinetic movement disorder, that is, characterized by the loss of movement.<\/div>\n
Highlight(blue<\/span>) – Clinical Presentation > Page 663 \u00b7 Location 6263<\/div>\n
Bradyphrenia,<\/div>\n
Highlight(blue<\/span>) – Clinical Presentation > Page 665 \u00b7 Location 6271<\/div>\n
Neuropsychiatric difficulties range from issues with impulse control (often worsened by dopamine agonist therapy used to treat PD; see page 339), anxiety, and depression to frank psychosis with hallucinations, memory loss, and dementia.<\/div>\n
Highlight(blue<\/span>) – Diagnosis > Page 666 \u00b7 Location 6284<\/div>\n
A favorable response to a levodopa challenge will clinch the diagnosis of PD and can often effectively rule out the atypical parkinsonisms (see page 342).<\/div>\n
Highlight(blue<\/span>) – Diagnosis > Page 666 \u00b7 Location 6286<\/div>\n
To reiterate, PD is a clinical diagnosis. MRI is not necessary in patients with classic symptoms and a good response to levodopa, but it may be useful to exclude secondary causes (see page 344) in patients with atypical presentations of the disease. More advanced MRI techniques, such as MR spectroscopy and diffusion tensor imaging, may offer higher sensitivity for detecting PD-related neurodegeneration, but their efficacy and diagnostic utility remain unknown. DaTscan, a specific type of single-photon emission computed tomography (SPECT) scan, enables visualization of dopamine transporter levels in the brain and can help distinguish patients with PD or atypical PD syndromes from patients with other diseases such as essential tremor. These scans cannot, however, distinguish between PD and atypical PD syndromes.<\/div>\n
Highlight(blue<\/span>) – Treatment > Page 667 \u00b7 Location 6298<\/div>\n
carbidopa, a dopa decarboxylase inhibitor that prevents the peripheral conversion of levodopa into dopamine. The combination of these two agents has been the basis of therapy for PD for<\/div>\n
Highlight(blue<\/span>) – Treatment > Page 667 \u00b7 Location 6305<\/div>\n
Other agents can be added as adjunctive treatment for patients who are no longer adequately responding to levodopa-carbidopa alone:<\/div>\n
Highlight(blue<\/span>) – Treatment > Page 667 \u00b7 Location 6306<\/div>\n
Dopamine agonists (pramipexole, ropinirole, or bromocriptine). These can cause sedation, lower extremity edema, and impulse control issues. MAO-B inhibitors (selegiline, safinamide, or rasagiline). Insomnia is a common side effect. COMT inhibitors (entacapone or tolcapone). COMT (Catechol-O-methyl transferase) is an enzyme that breaks down both dopamine and levodopa. COMT inhibitors therefore prolong the half-life of levodopa. They can cause gastrointestinal side effects, sleepiness, and urine discoloration (to dark yellow or orange; this is benign but can be upsetting if patients are not warned beforehand!). Liver function tests must be monitored in patients on tolcapone.<\/div>\n
Highlight(blue<\/span>) – Treatment > Page 669 \u00b7 Location 6325<\/div>\n
There is good evidence that starting exercise early, including balance and gait training, resistance and strength exercises, and aerobic exercise, can help patients maintain and often improve their motor function.<\/div>\n
Highlight(blue<\/span>) – Treatment > Page 669 \u00b7 Location 6329<\/div>\n
No pharmacologic treatment has yet been shown to alter the natural history of the disease.<\/div>\n
Highlight(blue<\/span>) – Prognosis > Page 671 \u00b7 Location 6339<\/div>\n
Despite maximal therapy, most patients will ultimately develop disabling complications. Dementia is common, affecting a significant minority of patients within 5 years. By 10 years, about 25% of patients will require nursing assistance, and average life expectancy from the time of diagnosis is less than 10 years.<\/div>\n
Highlight(blue<\/span>) – Tremor > Page 672 \u00b7 Location 6355<\/div>\n
Propranolol (a beta blocker) and primidone (an anticonvulsant) are the first-line drugs when medication is required, but they are typically only effective for mild cases.<\/div>\n
Highlight(blue<\/span>) – Tremor > Page 672 \u00b7 Location 6361<\/div>\n
13.8 For those of you with a good sense of timing, you may be able to discern that the tremor of ET is faster than the tremor of PD, typically 8 to 10 Hz (i.e., 8 to 10 cycles per second) compared with only 3 to 7 Hz.<\/div>\n
Highlight(blue<\/span>) – Tremor > Page 673 \u00b7 Location 6372<\/div>\n
common; patients with early PD are often initially thought to have essential tremor.<\/div>\n
Highlight(blue<\/span>) – The Atypical Parkinsonian Syndromes > Page 674 \u00b7 Location 6388<\/div>\n
major types of atypical parkinsonian syndromes are:<\/div>\n
Highlight(blue<\/span>) – The Atypical Parkinsonian Syndromes > Page 674 \u00b7 Location 6389<\/div>\n
Progressive supranuclear palsy Corticobasal degeneration Dementia with Lewy bodies Multiple system atrophy<\/div>\n
Highlight(blue<\/span>) – The Atypical Parkinsonian Syndromes > Page 675 \u00b7 Location 6394<\/div>\n
Magnetic resonance imaging (MRI) classically shows prominent midbrain atrophy resulting in what\u2019s known as the \u201chummingbird sign.\u201d<\/div>\n
Highlight(blue<\/span>) – Choreiform Disorders and Huntington Disease > Page 682 \u00b7 Location 6465<\/div>\n
St. Vitus dance<\/div>\n
Highlight(blue<\/span>) – Tardive Dyskinesia > Page 686 \u00b7 Location 6518<\/div>\n
monoamine neurotransmitters include dopamine, epinephrine, norepinephrine, and serotonin;<\/div>\n
Highlight(blue<\/span>) – Myoclonus > Page 689 \u00b7 Location 6537<\/div>\n
Hiccups (diaphragmatic myoclonus) and hypnic myoclonus (the sudden jerk many people get just as they are starting to fall asleep) are examples of physiologic myoclonus.<\/div>\n
Highlight(blue<\/span>) – Sleep-Related Movement Disorders > Page 691 \u00b7 Location 6566<\/div>\n
hypnic myoclonus, the myoclonic jerks that accompany falling asleep or transitions from one stage of sleep to another.<\/div>\n
Highlight(blue<\/span>) – CASE 13: FOLLOW-UP > Page 693 \u00b7 Location 6583<\/div>\n
Follow-up on Your Patient: You immediately suspect that Suzanne has Parkinson disease because of her shuffling gait and unilateral resting tremor. Your examination also reveals cogwheel rigidity in her right upper extremity and a positive pull test. Her cognitive testing is normal. You tell her she has Parkinson disease and discuss starting treatment with levodopa-carbidopa. Because her symptoms are interfering with her work in the hospital, she agrees and begins treatment immediately. One month later in follow-up she reports that the medication has helped her immensely and she has been able to continue working much as she has become accustomed to. You arrange to see her on a regular basis to monitor her symptoms and medication.<\/div>\n
Highlight(blue<\/span>) – CASE 13: FOLLOW-UP > Page 693 \u00b7 Location 6590<\/div>\n
How to diagnose and treat patients with Parkinson disease. The mnemonic TRAP (commit this to memory!) that summarizes the basic manifestations of Parkinson disease.<\/div>\n
Chapter 14 Neurocritical Care<\/div>\n
Highlight(blue<\/span>) – Cerebral Edema > Page 698 \u00b7 Location 6627<\/div>\n
Vasogenic edema is caused by the breakdown of the blood-brain barrier.<\/div>\n
Highlight(blue<\/span>) – Cerebral Edema > Page 699 \u00b7 Location 6634<\/div>\n
Cytotoxic edema is the result of cell death.<\/div>\n
Highlight(blue<\/span>) – Physiology > Page 702 \u00b7 Location 6667<\/div>\n
CSF<\/div>\n
Chapter 15 Altered Mental Status<\/div>\n
Highlight(blue<\/span>) – CASE 15 > Page 733 \u00b7 Location 6892<\/div>\n
Altered mental status (AMS)<\/div>\n
Highlight(blue<\/span>) – Encephalopathy Versus Aphasia > Page 734 \u00b7 Location 6904<\/div>\n
Like AMS, encephalopathy is a vague term that is often defined as any sort of \u201cbrain malfunctioning.\u201d<\/div>\n
Highlight(blue<\/span>) – Neurologic Causes of AMS > Page 736 \u00b7 Location 6938<\/div>\n
postictal<\/div>\n
Highlight(blue<\/span>) – Non-Neurologic Causes of AMS > Page 744 \u00b7 Location 7067<\/div>\n
Vladimir Nabokov1, author of Lolita, Ada, and Pale Fire, and physicist Richard Feynman are both believed to have been synesthetes.<\/div>\n
Highlight(blue<\/span>) – Non-Neurologic Causes of AMS > Page 745 \u00b7 Location 7079<\/div>\n
hyponatremia,<\/div>\n
Highlight(blue<\/span>) – Non-Neurologic Causes of AMS > Page 745 \u00b7 Location 7083<\/div>\n
is no<\/div>\n
Highlight(blue<\/span>) – Non-Neurologic Causes of AMS > Page 746 \u00b7 Location 7097<\/div>\n
pica behaviors (eating items not normally considered food, such as dirt or grass)<\/div>\n
Highlight(blue<\/span>) – Non-Neurologic Causes of AMS > Page 746 \u00b7 Location 7099<\/div>\n
chelation<\/div>\n
Highlight(blue<\/span>) – CASE 15: FOLLOW-UP > Page 751 \u00b7 Location 7160<\/div>\n
AMS.<\/div>\n
Note – CASE 15: FOLLOW-UP > Page 751 \u00b7 Location 7160<\/div>\n
Altered mental state.<\/div>\n
Chapter 16 Neuro-Oncology<\/div>\n
Highlight(blue<\/span>) – A Quick Word on Mass Lesions > Page 754 \u00b7 Location 7184<\/div>\n
Brain tumors are mass lesions: they take up space inside the skull.<\/div>\n
Highlight(blue<\/span>) – A Quick Word on Mass Lesions > Page 755 \u00b7 Location 7193<\/div>\n
Because the brain atrophies over time, older patients tend to have more space inside their skull and can therefore \u201chide\u201d mass lesions for longer<\/div>\n
Highlight(blue<\/span>) – A Quick Word on Mass Lesions > Page 755 \u00b7 Location 7194<\/div>\n
than younger patients, who have very little extra space and tend to become symptomatic earlier.<\/div>\n
Highlight(blue<\/span>) – Primary Brain Tumors > Page 756 \u00b7 Location 7208<\/div>\n
Primary brain tumors (i.e., tumors that originate in the brain) are actually significantly less common than metastatic brain tumors (i.e., tumors that originate elsewhere in the body).<\/div>\n
Highlight(blue<\/span>) – CASE 16: FOLLOW-UP > Page 779 \u00b7 Location 7449<\/div>\n
nicardipine<\/div>\n
Chapter 18 The Cranial Nerves<\/div>\n
Bookmark – Cranial Nerve Basics > Page 813 \u00b7 Location 7766<\/div>\n
Highlight(blue<\/span>) – Brainstem Reflexes > Page 817 \u00b7 Location 7811<\/div>\n
The pathway below explains why it\u2019s a consensual reflex: that is, why, if you shine light in one eye, both eyes will constrict.<\/div>\n
Index<\/div>\n
Highlight(blue<\/span>) – Page 906 \u00b7 Location 9342<\/div>\n
Parkinson disease (PD)<\/div>\n<\/div>\n","protected":false},"excerpt":{"rendered":"

Notebook Export The Only Neurology Book You’ll Ever Need Thaler, Alison I.; Thaler, Malcolm S. Citation (MLA): Thaler, Alison I., and Malcolm S. Thaler. The Only Neurology Book You’ll Ever Need. Wolters Kluwer Health, 2021. Kindle file. Chapter 1 Let\u2019s Get Started: Your Neurologic Toolbox Highlight(blue) – CASE 1 > Page 23 \u00b7 Location 337 … <\/p>\n

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