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The Only Neurology Book You’ll Ever Need
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’s Get Started: Your Neurologic Toolbox
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In a broad sense, all disease is experienced through the nervous system.
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It’s all in your head, whether it’s mental confusion or a skinned knee.
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communicate, whereas
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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).
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“apraxic.”
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Nasolabial fold flattening
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They decussate (or cross) in the medulla at the medullary pyramids, right where the brainstem meets the spinal cord;
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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.
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Dopamine depletion within the basal ganglia, for instance, as in Parkinson disease, can result in tremor and bradykinesia (slowness of movement).
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Extrapyramidal dysfunction is responsible for many of the manifestations of Parkinson disease, including tremor, abnormal posture, and gait dysfunction.
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“confrontation testing.”
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eyes closed, patients can only rely on proprioception, so if proprioception is impaired, they will lose their balance.
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dysmetria.
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Ataxic gait.
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Shuffling gait.
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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.
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where, anatomically, they come from (or, in neurologist speak, “localize to”).
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LP, EEG, and EMG/ NCS—form the crux of the diagnostic toolbox for neurologic disease.
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Radiologists use the term “intensity” as opposed to “density” to describe brightness on an MRI: things that appear bright are referred to as “hyperintense” (or “increased signal”), and things that appear dark are “hypointense” (or “decreased signal”).
Chapter 2 Stroke and Cerebrovascular Disease
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this is why posterior communicating artery aneurysms can cause third nerve palsies!
Chapter 3 Headache
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cytokines.
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Trigeminal Autonomic Cephalalgias (TACs)
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Trigeminal nerve distributions: V1 (ophthalmic), V2 (maxillary), V3 (mandibular).
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SUNCT (short-lasting unilateral neuralgiform headache with conjunctival injection and tearing) and SUNA (short-lasting unilateral neuralgiform headache with autonomic symptoms).
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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’s hair, or shaving. SUNCT presents with both conjunctival injection and tearing;
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Lamotrigine
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Preventive Treatment Lamotrigine Indomethacin Verapamil, Galcanezumab Indomethacin
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diagnosis, in reality very few headaches are directly associated with acute or chronic sinusitis.
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Pain around the sinuses, without evidence of an upper respiratory infection, is rarely a sinus headache, but far more often a manifestation of migraine.
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Trigeminal Neuralgia
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(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).
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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
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Secondary TN.
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This refers to TN caused by an underlying disease,
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Carbamazepine and oxcarbazepine are commonly used treatments for classical and idiopathic TN.
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gabapentin
Chapter 7 Neurocognitive Disorders and Dementia
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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.
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allele.
Chapter 13 Parkinson Disease and Other Movement Disorders
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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.
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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:
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akinesia for the often more accurate bradykinesia).
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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.
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unilaterally and then spreads contralaterally over a course of months to years.
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To be clear, though, don’t 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.
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Bradyphrenia,
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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.
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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).
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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.
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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
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Other agents can be added as adjunctive treatment for patients who are no longer adequately responding to levodopa-carbidopa alone:
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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.
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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.
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No pharmacologic treatment has yet been shown to alter the natural history of the disease.
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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.
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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.
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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.
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common; patients with early PD are often initially thought to have essential tremor.
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major types of atypical parkinsonian syndromes are:
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Progressive supranuclear palsy Corticobasal degeneration Dementia with Lewy bodies Multiple system atrophy
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Magnetic resonance imaging (MRI) classically shows prominent midbrain atrophy resulting in what’s known as the “hummingbird sign.”
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St. Vitus dance
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monoamine neurotransmitters include dopamine, epinephrine, norepinephrine, and serotonin;
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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.
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hypnic myoclonus, the myoclonic jerks that accompany falling asleep or transitions from one stage of sleep to another.
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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.
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How to diagnose and treat patients with Parkinson disease. The mnemonic TRAP (commit this to memory!) that summarizes the basic manifestations of Parkinson disease.
Chapter 14 Neurocritical Care
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Vasogenic edema is caused by the breakdown of the blood-brain barrier.
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Cytotoxic edema is the result of cell death.
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CSF
Chapter 15 Altered Mental Status
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Altered mental status (AMS)
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Like AMS, encephalopathy is a vague term that is often defined as any sort of “brain malfunctioning.”
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postictal
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Vladimir Nabokov1, author of Lolita, Ada, and Pale Fire, and physicist Richard Feynman are both believed to have been synesthetes.
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hyponatremia,
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is no
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pica behaviors (eating items not normally considered food, such as dirt or grass)
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chelation
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AMS.
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Altered mental state.
Chapter 16 Neuro-Oncology
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Brain tumors are mass lesions: they take up space inside the skull.
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Because the brain atrophies over time, older patients tend to have more space inside their skull and can therefore “hide” mass lesions for longer
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than younger patients, who have very little extra space and tend to become symptomatic earlier.
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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).
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nicardipine
Chapter 18 The Cranial Nerves
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The pathway below explains why it’s a consensual reflex: that is, why, if you shine light in one eye, both eyes will constrict.
Index
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Parkinson disease (PD)